Case Studies Important Environmental - Risk - v1

Adam Pawełczyk
František Božek
Marian Żuber
ENVIRONMENTAL RISK
CASE STUDIES
CZECH-POL TRADE
Prague 2018
Reviewers
Chris van KEER – University of Leuven, Belgium
Zoltan ZAVARGO – University of Novi Sad, Republic of Serbia
Cover design
Piotr ŻUBER
All parts of this publication are protected by copyright law. It must not be used
in any way without the consent of the Publisher. In particular, it must not be copied,
translated, reproduced on microfilm or stored in or processed by electronic systems.
All violations will be prosecuted.
© Copyright by Adam Pawełczyk, Wrocław 2018
ISBN 978-80-907124-0-9
Contents
List of Abbreviations .......................................................................................................................... 5

1. Preface .......................................................................................................................................... 7
2. Introduction to the risk assessment ............................................................................................... 9
2.1. Overview ............................................................................................................................. 9
2.2. Hazard identification ........................................................................................................... 11
2.3. Exposure assessment ........................................................................................................... 12
2.4. Dose–response assessment .................................................................................................. 15
2.4.1. Toxic substances ........................................................................................................ 15
2.4.2. Carcinogens ............................................................................................................... 17
2.5. Risk characterization ........................................................................................................... 20
2.6. Uncertainty analysis ............................................................................................................ 21
3. Cases overview ............................................................................................................................. 23
4. Analytical methods ....................................................................................................................... 27
5. Occupational risk posed by soil contaminants .............................................................................. 31
5.1. Background ......................................................................................................................... 31
5.2. The site characterization ...................................................................................................... 32
5.3. Starting data ........................................................................................................................ 33
5.4. Hazard identification and toxicity assessment ..................................................................... 36
5.5. Toxicity profiles of the studied contaminants ...................................................................... 39
5.7. Determination of dose–response relation ............................................................................ 49
5.10. Conclusions ......................................................................................................................... 55
6. Environment polluted with chromium .......................................................................................... 57
6.1. Background ......................................................................................................................... 57
6.2. The site description ............................................................................................................. 60
6.3. Health risk assessment ......................................................................................................... 61
6.3.1. Exposure assessment ................................................................................................. 62
6.3.2. Dose–response relation .............................................................................................. 65
6.3.3. Uncertainty analysis and discussion .......................................................................... 67
6.4. Conclusions ......................................................................................................................... 68
7. Nitrogen compounds in the surface waters ................................................................................... 69
7.1. Background ......................................................................................................................... 69
7.2. Sampling spot ...................................................................................................................... 70
7.3. Results of water analyses ..................................................................................................... 71
7.5. Determination of dose–response relation ............................................................................ 73
4
7.7. Hazard characterization ....................................................................................................... 76

7.9. Conclusions ......................................................................................................................... 78
8. Persistent organic pollutants in drinking water supply system ...................................................... 79
8.1. Background .......................................................................................................................... 79
8.2. Results of water analyses ..................................................................................................... 81
8.4. Determination of dose–response relation ............................................................................. 84
8.5. Dose–carcinogenic response relation ................................................................................... 85
8.6. Dose–non-carcinogenic response relation ........................................................................... 86
8.8. Exposure assessment for carcinogenic effects ..................................................................... 87
8.9. Exposure assessment for non-carcinogenic effects .............................................................. 89
8.10.1. Cancer risk characterization ..................................................................................... 90
8.10.2. Characterization of non-cancerous health effects chances ....................................... 92
8.12. Conclusions ......................................................................................................................... 93
9. Asbestos in the ambient air ........................................................................................................... 95
9.1. Background .......................................................................................................................... 95
9.3. Determination o dose–response relation .............................................................................. 98
9.6. Uncertainty in risk assessment ............................................................................................. 105
9.7. Conclusions ......................................................................................................................... 106
10. Summary ....................................................................................................................................... 109
11. References ..................................................................................................................................... 111
List of Figures ..................................................................................................................................... 119
List of Tables ...................................................................................................................................... 121
About the Authors ............................................................................................................................... 123
List of Abbreviations
AD – Adults Exposure Duration

ADAF – Age Dependent Adjustment Factor
ADD – Average Daily Dose
AT – Averaging Time
ATSDR – Agency for Toxic Substances and Disease Registry
BW – Body Weight
CALEPA – California Environmental Protection Agency
CDI – Chronic Daily Intake
CERCLA – Congress Enacted the Comprehensive Environmental Response,
Compensation, and Liability Act
COPs – Organochlorine Pesticides
CPS – Carcinogenic Potency Strength
CSF – Cancer Slope Factor
CSFo – Oral Cancer Slope Factor
CSFi – Inhalation Cancer Slope Factor
EC – Exposure Concentration
ED – Exposure Duration
EF – Exposure Frequency
ELCR – Excess Lifetime Cancer Risk
ET – Exposure Time
HEAST – Health Effects Assessment Summary Tables
HI – Hazard Index
HQ – Hazard Quotient
IARC – International Agency for Research on Cancer
IR – Intake Rate
IRIS – Integrated Risk Information System
IUR – Inhalation Unit Risk
LADD – Lifetime Average Daily Dose
LOAEL – Lowest Observed Adverse Effect Level
MCL – Maximum Contaminant Level
MF – Modifying Factor
MHC – Ministry of Health Care
MPC – Maximum Permissible Concentration
MRE – Maximum Residential Exposures
NDEP – Nevada Division of Environmental Protection
NOAEL – No Observed Adverse Effect Level
OEHHA – Office of Environmental Health Hazard Assessment
6 List of Abbreviations
PCBs – Polychlorinated Biphenyls

PCM – Phase Contrast Microscopy
PCOM – Phase-Contrast Optical Microscopy
POPs – Persistent Organic Pollutants
RAIS – Risk Assessment Information System
RfC – Reference Concentration
RfD – Reference Dose
UF – Uncertainty Factor
URF – Unit Risk Factor
US EPA – US Environmental Protection Agency
WHO – World Health Organization
1. Preface
Environmental risk is actual or potential hazard for living organisms and other ele-
ments of the environment that may exhibit adverse effects caused by effluents, emis-
sions and waste materials, arising from human activities. Assessment of the health risk is
a procedure within a scope of the environmental risk assessment. Estimation of the
health risk comprises qualitative and quantitative evaluation of the human’s exposure to
environmental contamination. On this basis probability of manifestation of adverse
health effects in a population is determined. This work deals with the topics of assess-
ment of risk for human health arising from environmental contamination.
Procedures of the environmental health risk assessment had been developed in the
1980s as a part of a Federal government effort to clean up land in the United States
that was contaminated by hazardous waste and that was identified by the US
Environmental Protection Agency (EPA). The program was created when Congress
Enacted the Comprehensive Environmental Response, Compensation, and Liability
Act (CERCLA).
Until that time the primary method of environmental hazard evaluation consisted
in comparing the real contamination level with pollutants’ permissible concentrations
in the air, water and soil. The highest permissible concentrations of the pollutants in
the environment have been set out by the governments of particular countries in order
to protect humans from possible exposition to harmful substances found in the air,
water and soil.
Such an approach however, does not reflect the real health hazard level that the
people are facing during their contact with the environment. In fact, the probability of
health effects incidences caused by the pollutants depends not only on the arbitrarily
adopted permissible concentrations but most of all on the exposure scenarios of the
population considered. It is only the full analysis of actual health risk that shows real
effects of the polluted environment on humans.
This book presents cases of the air, water and soil pollution with harmful sub-
stances, both toxic and mutagenic, and gives examples of hazard’s estimation as well
as health risk assessment in different exposure scenarios. Residential and occupational
scenarios are mostly taken into account. They include all elements of the procedure
starting from hazard identification, followed by exposure assessment, determination of
8 Chapter 1
dose-response relation, risk characterization and ending with uncertainty analysis.

Also some recommendations in a concise manner are given aiming at hazard as well
as health risk abatement.
The presented examples involve real, independent cases that were subjects to gov-
ernmental grants and commercial projects. The cases aim to help the reader to under-
stand more clearly different calculation methodologies and to carry out the risk as-
sessment in different environments. The work focus are exclusively anthropogenic
emissions released as a result of routine commercial businesses, municipal activities as
well as technical disasters affecting human health and well-being. It should be stressed
that there exist examples of the environmental pollution where, so far, no precise risk
assessment is possible due to the lack of necessary data or reliable estimation proce-
dures. Such a case could be contamination with petroleum products which usually
constitute a mixture of hundreds chemical compounds of different chemical, physical
and toxicological properties.
This book is intended as a selection of the representative cases describing risk es-
timation procedures, aimed at students, professionals and other users interested in
disciplines ranging from environmental engineering and environmental chemistry to
environmental safety and all areas of environmental science where human health and
well-being are involved.
Adam Pawełczyk
This work was carried out at the Wrocław University of Science and Technology,
Poland within the scientific funds allocated for statutory activities 0401/0200/17 by
the Ministry of Science and Higher Education.
2. Introduction to the risk assessment
2.1. Overview
The commonly accepted approach of environmental hazard assumes comparison of

the real measured level of particular contaminants in the ambient environment with
permissible pollution standards, set by the obligatory law regulations. In Poland the
standards established by the Ministry of Environment control the pollution levels in
the air, waters and soils (ME 2001). Additionally, for the purpose of the degraded
grounds remediation, specific standards for soils and earth quality were laid down
(ME 2002).
In the USA and some Western European countries environmental health risk as-
sessment procedures have been implemented, enabling to determine probability of oc-
currence of adverse health effects, resulting from the human’s exposure to the contami-
nated sites. This assessment constitutes a part of the risk management and is applied for
establishing the strategy and actions aiming at the risk abatement (Wcislo 2003). The
most applicable method of the risk reduction involves both the environment cleaning
and harmful substances neutralization. Second possibility is elimination of exposure
pathways. The third, most disputable way of the risk avoidance is limitation of the re-
ceptor’s access to the polluted area. It means that population from the polluted area has
to be evacuated or the polluted area declared as a restricted access zone.
For the purpose of the health risk assessment related to polluted areas and for
cleaning up projects a special federal government’s program has been declared in the
USA named “Superfund”. The program needed a particular procedure of the health
risk estimation which had not been developed at that time. The United States Envi-
ronmental Protection Agency – US EPA started works on development of methodo-
logical principles of the health risk assessment which could be an aid in taking any
measures and actions addressed the contaminated sites problem. The methodology has
been published in the Risk Assessment Guidance for Superfund (EPA 1989).
The methodology based on US EPA guidelines distinguishes the toxic and car-
cinogenic substances and recommends different approach in the risk assessment for
10 Chapter 2
both types of pollutants. Prior to the assessment procedure goal of the evaluation
should be defined. The procedure results can be used for the selection of remedy ac-
tions, arbitration proceedings or it can be just a cognitive research. The methodology
consists of the following main steps shown in Fig. 1: hazard identification, exposure
assessment, dose–response assessment, risk characterization and uncertainty analysis.
Fig. 1. Sequence of the stages of the health risk assessment
The first step is a part of toxicity assessment characterizing the chemicals in re-
spect of type and intensity of health effects resulted from the exposure to the chemi-
cals. It enables to reduce number of chemicals to be considered in the risk assessment.
This step may include data collection and evaluation and comparison of site contami-
nation with background and selects all data needed for use in the risk assessment.
Collection and evaluation of the data includes determination of humans’ contacts
with the harmful chemicals, magnitude of exposures to the chemicals that are present in
the environment and quantification of the exposure. The exposure exists only when three
of the following elements exist at the same time: the exposure source, the exposure
pathway and the receptor. This step usually takes into account current and future expo-
sures considering different exposure pathways: inhalation (air), ingestion (water, meat,
eggs, vegetables and dairy products) and dermal contact (contact with the soil, water,
Introduction to the risk assessment 11
etc). As the receptor, an individual is meant. A necessary part of the exposure assess-
ment is characteristics of the site and characteristics of the populations on the site.
Furthermore, quantification of exposure has to be conducted. The quantification
includes calculation of chemicals’ intakes by the individual for each exposure path-
way. The intakes are daily doses averaged over the lifetime or exposure duration, ab-
sorbed by a representative of certain population and are expressed in terms of the mass
of substance in contact with the body per unit body weight per unit time (e.g. mg
chemical substance per kg body weight per day – [mg/(kgday)]). Other approach con-
sists in determination of chronic concentration instead of average doses absorbed. This
refers mainly to inhalation exposure pathway. In this step an exposure scenario is very
important as it determines the exposure time, contact frequency etc. Three basic sce-
narios are considered:
 resident’s scenario,
 incidental/recreational contact scenario,
 occupational scenario.
Next, physiological exposure factors such as age and gender should be considered
depending on the type of population affected by the chemicals. These factors deter-
mine the body weight, contact frequency, the daily inhalation rate values, ingested
water, food etc. For example standard procedures applied for the exposure calculations
assume the body weight 78.1 kg for men, 65.4 kg for women and 16 kg for children of
age between 1 and 6 years (EPA 2000). Also daily water intake and inhalation rates
vary for different population groups.
The next step is determination quantitatively the relationship between the dose of
the contaminant absorbed and the frequency of adverse health effects among the ex-
posed population established. In the health risk assessment distinction between two
types of hazardous chemicals is made – toxic (non-carcinogenic) and carcinogenic.
This step is followed by discussion of the level of calculated risk and hazards. The
obtained figures are compared with commonly accepted risk levels. In the case of
unaccepted hazards some solutions may be proposed in order to reduce risk.
The risk assessment procedure ends with uncertainty analysis that is a discussion
of all possible inaccuracies and simplifying assumptions reflecting the calculated risk
values and risk characterization. More detailed data are given in the chapters present-
ing particular case studies.
2.2. Hazard identification
Hazard identification is a part of the whole procedure which is related to the identi-
fication if a substance present in the environment produces adverse health effects (e.g.,
cancer, allergy, birth defect) and whether the adverse health effects are likely to occur
12 Chapter 2
in humans. Type of the effects are recognized and their dependency on the level of
absorbed doses. Findings of this stage are a determining factor in the taking of a deci-
sion about further assessment steps.
2.3. Exposure assessment
Exposure assessment consists in determining doses of particular chemicals ab-

sorbed by the individuals over all pathways defined in the exposure scenarios. This
step requires precise data on the contaminants concentration and population structure,
especially when residents scenario is concerned. Calculations of the chemicals intake
transported into the individual’s body by different exposure pathways can be con-
ducted using equations recommended in the Risk Assessment Guidance for Superfund
(EPA 1989). The universal formula for calculation of the intake of chemical can be
expressed as:
I = C  CR  EFD/(BW  AT) (1)
where:
I – intake – amount of the chemical taken [mg(kg body weight)-1 d–1],
C – average concentration of the chemical over the exposure period, [mg/dm3
water], [mg/kg soil], [mg/m3 air], etc.,
CR – contact rate, amount of contaminated medium contacted per unit time,
[mg soil/d], [m3 water /d], [m3 air/d], etc.,
EFD – exposure frequency and duration. It describes how often and how fre-
quently exposure occurs [hours], [days], [years],
BW – average body weight [kg],
AT – averaging time, period over which exposure is averaged [d].
The exposure and risk assessment require establishing of exposure scenario models
adjusted to the site and population characteristics. The scenarios enable to adapt for-
mula (1) to the real cases of exposure, taking into consideration the following basic
exposure pathways:
 ingestion of the water polluted with chemicals,
 inhalation of air containing toxic or carcinogenic substances,
 inhalation of air polluted with airborne dust originating from soil dusting,
 inhalation of air contaminated with volatile chemical substances released from
the soil,
 consumption of vegetables and agricultural products grown on the polluted soil,
 consumption of meat and dairy products from animal breeding on the polluted area,
 incidental ingestion of the contaminated soil,
 dermal contact with the contaminated soil (EPA 1989).
One should be aware that much more exposure scenarios are possible. They in-
clude a combination of the above pathways and number of other variants, resulting
from the type of the receptor contact with the polluted medium. Thus, variety of spe-
cific formulas can be derived from the formula (1) enabling to calculate the chemicals
intake for variety of pathways and exposure scenarios. Below some most used exam-
ples are given which may vary when real conditions are applied, depending on par-
ticular exposure scenario (EPA 1989).
Intake of chemicals by ingestion with drinking water

The amount of chemicals ingested with drinking water can be calculated from the
formula:
I = Cw  IR  (EF  ED)/(BW  AT) (2)
where:
Cw – average concentration of the chemical in water over the exposure
period [mg/dm],
IR – ingestion rate – daily consumption of water [dm3/d],
EF – exposure frequency [d/y],
ED – exposure duration [y],
BW – average body weight [kg],
AT – averaging time, period over which exposure is averaged [d].
Intake of chemicals by inhalation with air

I = Ca  IR  ET  EF  ED/(BW  AT) (3)
where:
Ca – average concentration of the chemical in air over the exposure period
[mg/m3],
IR – inhalation rate [m3/h],
ET – exposure time [h/d],
the remaining symbols are the same.
Intake of chemicals by ingestion of contaminated fruits and vegetables

I = Cf  IR  FI  EF  ED/(BW  AT) (4)
where:
Cf – average concentration of the chemical in food [mg/kg],
IR – ingestion rate [kg/meal],
FI – fraction ingested from contaminated source – unitless,
EF – exposure frequency [meals/y],
ED – exposure duration [y].
14 Chapter 2
Similar formula is applied for calculations of the chemicals intake by ingestion of

contaminated meat, eggs and dairy products.
Intake of chemicals by accidental ingestion of contaminated soil

I = Cs  IR  CF  FI  EF  ED/(BW  AT) (5)
where:
Cs – concentration of chemical in soil [mg/kg],
IR – ingestion rate [mg soil/day],
CF – conversion factor [10–6 kg/mg],
EF – exposure frequency [d/y].
Absorbed dose of chemicals by dermal contact with the contaminated soil

I = Cs  CF  SA  AF  ABS  EF  ED/BW  AT (6)
where:
SA – skin surface area contacting with the soil [cm2/event],
AF – soil to skin adherence factor [mg/cm2],
ABS – absorption factor – unitless,
EF – exposure frequency [events/y].
The above examples illustrate some of cases from among numerous possibilities
reflecting variety of exposure scenarios.
When calculating the intakes particular concern should be devoted to considera-
tions of the exposure duration and averaging time. The standard exposure durations
and averaging times are classified as chronic, subchronic and shorter-term exposures.
Applying the proper exposure and averaging time values has great weight for correct-
ness of the whole risk assessment process. The averaging time which has to be chosen
for exposure calculations depends on the type of pollutant – carcinogenic or non-
carcinogenic – and on the type of toxic effect being assessed. Below the possible cases
are given:
Toxic (non-carcinogenic) chemicals

In the case of non-carcinogenic substances the intakes are always determined by
averaging them over the period of exposure, that is:
 developmental toxicants – when evaluation exposures to developmental toxi-
cants is made, intakes are calculated by averaging over the exposure event, for
instance over a day or a single exposure incident.
 acute toxic substances – for calculation of acute toxic substances intakes, the
shortest exposure period that could produce an adverse effect is used for aver-
aging. It is usually an exposure event or a day.
 longer term exposure to non-carcinogenic toxicants (developmental and acute)

– intakes are determined by averaging them over the period of exposure (i.e.,
subchronic or chronic daily intakes).
Generally the intake calculated in this way are called average daily dose (ADD).
Carcinogenic chemicals
For carcinogenic chemicals the intakes are calculated by proportional distribution
of the total cumulative dose absorbed, over a lifetime. It is assumed for carcinogens
that high doses of the chemicals absorbed by an individual over a short period of time
is equivalent to corresponding low doses spread over a lifetime (EPA 1986b). It means
that intakes are determined by averaging them over the lifetime, that is 70 years by
convention (70 years  365 days/year = 25 550 days, actually). Such averaged intakes
are called chronic daily intakes (CDI) or lifetime average daily doses (LADD).
2.4. Dose–response assessment
The dose–response assessment is a step in which toxicological and epidemiologi-

cal knowledge is involved. In this step toxicity of the chemicals contaminating the
environment is discussed and quantitatively relationship between the dose of the con-
taminant absorbed and the frequency of adverse health effects among the exposed
population established. For the purpose of the dose–response assessment, toxicity data
bases have been determined and published. The most useful are Integrated Risk In-
formation Systems (IRIS), Risk Assessment Information System (RAIS), Agency for
Toxic Substances and Disease Registry (ATSDR) and Health Effects Assessment Sum-
mary Tables (HEAST). Use of these data bases substantially simplifies the assessment
procedure. When no data are available, arduous, time consuming and very costly toxi-
cological and epidemiological investigations are needed which in many cases makes
the assessment impossible.
In the health risk assessment distinction between two types of hazardous chemicals
is made – toxic (non-carcinogenic) and carcinogenic.
2.4.1. Toxic substances
Toxic substances are believed to comply with the threshold theory of toxicity
while carcinogenic ones the linear theory. According to the threshold theory, a toxic
chemical must be present in an organism at some threshold concentration, or a threshold
dose must be absorbed before any adverse effects occur. It means that protective
16 Chapter 2
mechanisms are believed to exist in human organism that must be broken before the
adverse effect appears. Below the threshold concentration or dose, no such adverse
effects appear (Fig. 2).
Fig. 2. Threshold doses for toxic substances A, B and C
For evaluating the non-carcinogenic effects most often a “reference dose” (RfD)
applies for exposure periods between 7 years (approximately 10 percent of a human
lifetime) and a lifetime. RfD has been derived from the so called “no-observed-
-adverse-effect-level” (NOAEL), that is from highest concentration (or dose) of a toxic
substance, that produces no health effects yet. When the threshold concentration is
exceeded the adverse effect start to manifest. Similarly the so called “lowest-observed-
-adverse-effect-level” (LOAEL) is defined which is the lowest concentration (or dose)
of a toxic substance that manifest health adverse effects.
The RfD incorporates “modifying factor” (MF) taking into account limited quality of
data bases, extrapolation of doses from experimental models to real environmental condi-
tions and uncertainty connected with transferring experimental data from animals to hu-
mans. Additional “uncertainty factor” (UF) ranging from 0 to 10 is applied for purpose of
safety margin (EPA 1989). It reflects additional uncertainties in health assessment proce-
dure for non-carcinogenic substances. The RfD is calculated from:
RfD = NOAEL / (UF  MF). (7)
The unit for RfD is [mg/(kg  d)].
For such substances a non-probabilistic approach is used for evaluation of the poten-
tial health effects intensity. Instead, comparison of the absorbed dose by an individual
over a specified time period, with the reference dose RfD derived for a similar exposure
period is conducted. The calculated value is called a non-cancerous hazard quotient HQ
which expresses how many times the exposure level (the dose taken) exceeds the RfD.
In other words HQ stands for the ratio of the exposure estimate to a concentration or
dose, considered to represent a “safe” environmental concentration or dose RfD.
HQ = E/RfD (8)
where E – exposure level (intake).
The noncancer hazard quotient HQ assumes that there is a threshold level of expo-
sure RfD below which adverse health effects will not develop. If the exposure E ex-
ceeds this threshold (if E/RfD > 1), potential noncancer effects may occur. For consid-
eration of the possibility of adverse noncarcinogenic health effects, three standard
exposure durations are used:
– chronic (for humans they range in duration from 7 years to a lifetime),
– subchronic (from 2 weeks to 7 years),
– shorter-term exposures (less than 2 weeks).
It should be stressed that for evaluation of short-term exposures and potential non-
carcinogenic effects, subchronic or shorter-term, not chronic toxicity values RfD
should be used.
In the case of exposure to several noncarcinogenic substances, the potential for the
noncarcinogenic health effects is assessed in accordance with the principle of the cu-
mulative effect of the chemicals on the body, by calculating a hazard index HI, being a
sum of the hazard quotients determined for the individual substances:
HI = Σ HQi (9)
where: HQi – a hazard quotient for the i-th substance.
An HI exceeding 1 means that at a given exposure value harmful health effects
may arise. Generally the following hazard level thresholds are specified in the litera-
ture (Brebbia 2010):
HQ  1 – acceptable
HQ  (1; 4 – tolerable
HQ  4 – unacceptable.
The same values are valid for Hazard index HI.
2.4.2. Carcinogens
Carcinogenic substances are believed to comply with linear theory (Fig. 3) that
means that there are no threshold concentration levels safe for an individual. As
18 Chapter 2
opposed to toxic substances each dose of carcinogen, even lowest, may cause a can-
cer risk.
According to the classification developed by US EPA the following carcinogenic
group have been established:
A – carcinogenic to humans: agents with adequate human data to demonstrate
the causal association of the agent with human cancer (typically epidemio-
logic data).
B – probably carcinogenic to humans with two sub-groups:
B1 – agents with sufficient evidence from animal bioassay data, but either lim-
ited human evidence,
B2 – with little or no human data.
C – possibly carcinogenic to humans: agents with limited animal evidence and
little or no human data.
D – not classifiable as to human carcinogenicity: agents without adequate data
either to support or refute human carcinogenicity.
E – evidence of non-carcinogenicity for humans: agents that show no evidence
for carcinogenicity in at least two adequate animal tests in different species
or in both adequate epidemiologic and animal studies.
Fig. 3. Linear response to doses for carcinogenic substances X, Y and Z
Toxicity value for carcinogenic effects, or in other words a factor enabling to con-
vert the absorbed dose of human carcinogen into cancer risk composes the so called
“cancer slope factor” (CSF) or “carcinogenic potency strength” (CPS). The greater
slope, the strongest carcinogenic effect may be expected. As shown in Fig. 2 the sub-
stance “A” has the greatest carcinogenic potency strength. Slope factors are calculated
for carcinogens in classes A, B1, and B2 and are published in data bases of EPA. CFS is
mostly expressed in [(mg/(kg  d))–1].
Toxicity values for carcinogenic effects can also be expressed in terms of risk per
unit concentration of the chemical in the medium (air, water) being in contact with an
individual. These risks per unit concentrations are called unit risks or unit risk factors
(URF) and are calculated by dividing and multiplying the slope factor by standardized
figures representing body weight and ingestion/inhalation rates. To get URF for
ingestion of a substance with water, the oral cancer slope factor (CSFo) is divided by
70 kg (average adult body weight, as convention) and multiplied by 2 dm3/day (daily
water consumption). Similarly, the URF for inhalation contact is obtained by dividing
the inhalation cancer slope factor (CSFi) by 70 kg and multiplied by 20 m3/day (daily
air inhalation rate). Thus:
– water unit risk = risk per µg/dm3 = CSFo/70 (kg)2 [dm3/(day10–3)], and
– air unit risk = risk per µg/dm3 = CSFi/70 (kg)20 [m3/(day10–3)].
The multiplication factor 10–3 is used to convert the units. CSF is expressed in
[(mg/(kgday))–1] while the unit risk is given in [µg/dm3] – for water unit risk, or in
[µg/m3] – for air unit risk.
For cancer risks assessment, exclusively average lifetime exposure must be used.
On the other hand noncarcinogenic effects assessment is obligatory conducted using
short-term exposures.
The following linear relation is used for the low-dose carcinogenic risk quantifica-
tion (EPA 1999):
Risk = CSF  CDI (10)
where:
Risk – unitless cancer probability of developing cancer,
CSF – slope factor, expressed in [(mg/(kgday))–1].
CDI – chronic daily intake averaged over 70 years [mg/(kgday)] – ingested with
drinking water, by inhalation with air, by ingestion of contaminated fruits
and vegetables, by accidental ingestion of contaminated soil or by dermal
contact with the contaminated soil, etc. CDI is also called the lifetime av-
erage daily dose (LADD).
The linear equation (10) is valid only when low risk levels exist, that is below 0.01.
For higher exposure levels where higher risk is expected the following expression
is valid:
Risk = 1 – e–(CDICSF). (11)

20 Chapter 2
Cancer risk for multiple substances can be calculated from the following equa-
tion:
m
Risk t   Risk
i 1
i
(12)
where:
Riskt – the total cancer risk expressed as a unitless probability
Riski – the risk estimate for the i-th substance.
The calculated risk represents the probability of cancer incidence above the
natural level in the environment at particular site, caused by the contaminating
chemical.
In the original guidelines developed by Superfund, a carcinogenic risk range of
110–4 to 110–7 modified to 110–4 to 110–6 was recommended as a target risk level.
Thus, the ambient chemical concentrations should be reduced to the levels providing
at least the risk within the above mentioned limits (EPA 2015c; Kelly 1991).
The National Contingency Plan in the USA designated 10–6 as a starting point for
discussion of acceptable target risk at a site or as a “point of departure” (EPA 2015d).
This problem has generated a lot of debate in scientific papers and it still arouses con-
troversies. Nevertheless, 10–6 is now generally regarded by literature as acceptable and
safe (Callahan 2004).
In general, the US EPA considers cancer risks that are below 1 chance in 1 000 000
(1 × 10–6 or 1E–06) to be so small as to be negligible, and risks above 1E–04 to be suffi-
ciently large that some sort of remediation is desirable. Excess cancer risks that range
between 1E–06 and 1E–04 are generally considered to be acceptable.
2.5. Risk characterization
Risk characterization is an integral element of the risk assessment procedure for

both ecological and health risks. The purpose of risk characterizations is to interpret
the risk calculations and available data coming from observations and explain their
meaning for the health of populations. Characterization is a kind of discussion and
summarization of the whole assessment process which helps users understand findings
of the risk estimation.
An important part of the risk characterization is comparison of the risk and
hazard levels with generally accepted international acceptable target risks (Calla-
han 2004, Brebbia 2010). The risk characterization is an essential component of
the risk assessment process that supports judgment aiming at the risk abatement
actions.
2.6. Uncertainty analysis
The risk assessment procedure must absolutely end with uncertainty analysis that
is a discussion of all possible inaccuracies and simplifying assumptions reflecting the
calculated risk values and risk characterization. The uncertainties result from limita-
tions of the toxicity information for many of the chemicals. The toxicity values are
derived from experiments conducted with animals and extrapolated on human organ-
isms. Consequently, there are varying degrees of uncertainty associated with the tox-
icity values calculated. The exposure parameters used in these risk calculations
(hours/day, days/year) are based on some scenario assumptions which in many cases
are not very accurate. Additionally it is not known whether concentrations of the
harmful contaminants in the environment remain at a constant level over the whole
lifetime of the individuals belonging to a given population. Usually the exposed hu-
man population is very diverse with respect of the gender, age, individual factors, and
physiology. This reflects the daily inhalation, water and food ingestion which affects
the contaminating chemical intake dose.
Also the sampling conditions are quite often not uniform in regard to the weather
conditions at sampling sites. The concentrations may vary significantly depending on
the weather parameters, and protective measures taken, which can lead to some un-
certainty in the derived health risk values. Due to the simplifications and ambiguities
the obtained results cannot be regarded as definite and absolute.
For reduction of the uncertainties computer-aided simulations have been imple-
mented. They enable to carry out sensitivity analysis of the final results and to identify
the crucial exposure pathways. Such extensive opportunities in evaluation of the un-
certainty and variability associated with risk assessments for contaminated sites gives
the Monte Carlo analysis (Hayse 2000). The probabilistic approach to the risk assess-
ment with the use of Monte Carlo simulation involves the computational parameters in
form of value distributions instead of point values. Thus, the Monte Carlo approach
makes it possible to analyze the health risk in form of distribution curve providing the
assessors with information about the relation risk level – population percentage con-
cerned.
The following sections present case studies related to the real conditions and as-
sessment procedures adapted and developed in frame of the authors’ research projects.
The above risk assessment procedures were applied with modifications and adjust-
ments necessary to estimate and characterize the exposure and risk associated with
environment contamination with organochlorine compounds, asbestos and nitrogen
compounds. The contaminants origin represents all types of the pollution sources de-
scribed in chapter 1, that is the running production (1-st type of source), stored waste
materials and accumulated harmful products (2-nd type of source) and emission as
a consequence of accidents (3-rd type of source).
22 Chapter 2
A few words should be devoted to the cases related to the environment pollution
with complex mixtures, petroleum products, for instance. So far, there was no precise
risk quantification method developed for such systems. This is due to lack of adequate
knowledge about the movement of petroleum components in soil and shortage of data
about the toxicity of the components. The available analytical methodology does not
provide adequate information necessary to evaluate the health risks posed to humans
by the mixtures of complex nature (Grabas et al. 2015; Heath et al. 1993; Pawełczyk
et al. 2017a; Todd et al. 1999).
Thus, health risk assessment in those cases is rather impossible. Some approaches
consist in defining reference compounds of relatively well characterized toxicity for
a range of compounds. For example, for unsaturated compounds, one reference RfD
was identified for all compounds C9 through C32. For this group of hydrocarbons
pyrene was accepted as reference compound with RfD 0.03 mg/kg/day (Hutcheson
et al. 1996).
3. Cases overview
Case studies presented in this book cover different instances of the environment
polluted with harmful substances that found their way to air, waters and soils on mili-
tary and civilian areas. A brief profiles of particular cases are presented hereafter.
As mentioned in the preface, exclusively man-made emissions that happened as
a consequence of routine commercial businesses, municipal activities as well as tech-
nical disasters affecting human health and well-being have been considered (Yung-Tse
Hung et al. 2012; Maciejewski and Żuber 2006).
Occupational risk posed by soil contaminants. The case study concerns estimation
of the health risk in the occupational scenario on a delimitated property intended for
railway carriage service station. The estimation comprises assessment of ground con-
tamination data, toxicological assessment of the identified anthropogenic pollutants,
identification of the environmental hazard, exposure assessment in the occupational
scenario, estimation of dose-response relation, risk characterization and uncertainty
analysis.
The assessment comprises qualitative and quantitative determination of the humans
exposure to environmental contamination. On this basis probability of manifestation of
adverse health effects in a population is determined.
In the procedure of occupational health risk assessment an exposure to upper layer
of the polluted soil was taken into account. Inhalation route of exposure was not con-
sidered because there were no circumstances for the presence of harmful anthropo-
genic substances in the air in significant concentrations. Ground waters had not been
taken into consideration, as well, for in the assumed scenarios no contact of the station
staff occurs with this exposure source.
Chromium in the environment. In this case study the results of water, soil and air
analyses sampled in the vicinity of a former ferrochromium metallurgical plant. In the
past, the area was used for the disposal of waste materials containing smelter slag, dust
and other waste products from the manufacture of ferrochromium alloys for the army.
In nineties, the production was abandoned and a project aimed at the liquidation of the
dump had been initiated. The project concentrated on the recovery of chromium re-
mains and the utilization of the leftover material as a road construction aggregate.
24 Chapter 3
Based on the analyses of ground water, soil and air, a health risk caused by environ-
mental pollution with chromium, especially with Cr(VI), was determined for residen-
tial and occupational scenarios. It was found that the level of chromium emissions to
the environment constitutes a potential danger of toxic and carcinogenic cases in hu-
mans exposed to the emission in the affected area. An increased level in the hazard
quotient has been observed in the case of occupational activities. As far as the muta-
genic effects are concerned, the occupational inhalation exposure was found to be very
high, which may raise extreme concern about carcinogenic risk.
Surface waters contaminated with nitrogen compounds. Results of analyses of
water in the river Mała Panew in South West Poland have been reported. The river
flows through a rural area with some chemical industry developed. Aim of the work
was to investigate the pollutants level in the river, compare the obtained results with
obligatory drinking water standards and determine possible health effects when using
the river as a source for drinking water production. Attention was put to nitrogen
compounds as nitrate(V) ions (NO3−) and nitrite(III) ions (NO2−), mostly of anthropo-
genic origin were detected in the monitored water. The average concentrations of the
NO3– and NO2– were 3.54 mg/dm3 and 0.286 mg/dm3, respectively. The chances for
non-carcinogenic effects, namely methemoglobinemia, resulting from possible expo-
sure to the examined chemicals were determined based on the analytical and toxico-
logical data. Since infants are the subpopulation most susceptible to nitrate induced
methemoglobinemia, the assessment was limited to children aged 0–3 years. The de-
termined values expressed by hazard quotient (HQ) and hazard index (HI) indicate
that the water pollutants and their concentrations do not exceed unity, however in the
case of infants, the other nitrate sources should be controlled.
Polychlorinated biphenyls in drinking water. This case study refers to water in-
takes providing one of the districts located near the city of Wrocław with drinking
water. Surprisingly high concentrations of polychlorinated biphenyls (PCBs) and or-
ganochlorine pesticides (COPs), classified as persistent organic pollutants (POPs),
were detected in the monitored sites. Based on the analytical and toxicological data,
the individual health risks in respect to carcinogenic effects (excess cancer risk over
a lifetime) in humans were assessed, resulting from direct ingestion of community
water. Non-carcinogenic effects resulting from exposure to the examined POPs were
determined, as well. The conservative approach to risk assessment, taking into account
a safety margin for data incompleteness, was adopted. The carcinogenic risk was
found to slightly exceed the unconditionally acceptable risk of 10–6 in the case of
polychlorinated biphenyls and hexachlorocyclohexane (HCH), for all the inhabitant
populations. The determined values of non-carcinogenic effects expressed by hazard
quotient (HQ) and hazard index (HI) indicate that the water pollutants and their con-
centrations do not cause an increase in non-carcinogenic incidences in the inhabitants
using the monitored water sources.
Cases overview 25
Asbestos in the air. This case study refers to an assessment of human health risk
associated with the air pollution with asbestos respirable fibers in towns of the south-
west Poland. The aim of the work was to determine if any prevention measures would
be necessary to reduce the exposure of populations to the air pollutant. The risk as-
sessment was carried out based on the air analyses and latest asbestos toxicity data
published by the Environmental Protection Agency (US EPA), USA and Office of
Environmental Health Hazard Assessment (OEHHA). It was found that in some sites
the concentration of the asbestos fibers exceeded the acceptable levels, however it
does not result in worrying health risk increase, even when the resident exposure sce-
nario is taken into consideration. The highest asbestos fibers’ concentration was found
in the air in the town centers during rush hours. In three spots however, the calculated
maximum health risk exceeded 1E–04 which is generally considered high according to
US EPA standards.
4. Analytical methods
Chromium in the soil

The Polish Standard (PS, 1984) was adapted for sampling using a Quick Take 30
aspirator with an electronic flow control adjustment at the flow rate of 16.0 L/min and
with 180 minutes sampling time applied. The air stream was filtered on Sartorius cel-
lulose nitrate membrane filters with 25 mm diameter and 0.4 µm pores. After sam-
pling, the filters were protected in plastic boxes and delivered to the laboratory.
Analyses of chromium in the samples were carried out by the ICP method using an
ICP-MS spectrometer Elan 9000 Perkin Elmer. For mineralization of the samples,
pressure decomposition in nitric acid and hydrogen peroxide was applied by the use of
a microwave mineralizer Anton-Paar PE Multiwave 3000.
For the analysis of hexavalent chromium, a procedure described in Ashley et al.
(2003) was applied. Ion chromatography was used to separate Cr(VI). The equipment
consisted of an HPLC PE series 200 with UV-Vis 785A and FD200, IC Dionex DX-120.
The mobile phase flow rate was 1.0 cm3/min, a post-column reagent flow rate was
0.7 cm3/min, and a post-column tube length was 2.2 m. The extraction was made with
a 2% NaOH and a 3% Na2CO3 solution in deionized water. The mobile phase was
250 mM (NH4)2SO4 and 100 mM NH4OH.
The detection limit of chromium(VI) in the case of air samples was 0.004 μg per
sample. For the ground water, it was about 1 μg/L, and for soil, it was about 5 μg/kg.
Polychlorinated biphenyls in water

The adapted analytical procedures according to the Polish Standards (PS 2002)
were applied for determination of the examined pollutants in water. After a standard
solution was added, double extraction with n-hexane was performed. Each sample was
purified by adding sulfuric acid, shaking and separating the layers. The extract was
dried by filtering it through a layer of sodium sulfate into a round-bottom flask, and
concentrated (Pawełczyk et al. 2008).
Then a potassium hydroxide solution was added, the sample was heated and ethyl
alcohol was introduced. After re-shaking the n-hexane layer was separated. The ex-
tracted and purified samples were analyzed using an M504 gas chromatograph
28 Chapter 4
equipped with an HP5 capillary column and an ECD electron capture selective to-
wards organochlorine compounds. To heighten the detectability range sensibility of
the apparatus was adjusted. The chromatograph’s operating parameters are shown in
Table 1.
Table 1. Parameters of chromatographic apparatus
Parameter Value/type
column length 60 m
column temperature:
 initial 160 °C
 temperature rise 5 °C/min
 final 325 °C
initial isotherm 1 min
final isotherm 15 min
carrier gas nitrogen
doping gas nitrogen
Hydrocarbons in water and soil

Benzene, toluene, ethylbenzene and xylene (BTEX) were determined using a head-
space gas chromatographic method. 0.5 dm3 of the water sample was extracted with
1 cm3 of n-pentane in a micro extraction flask according to the Polish Standard
PN-85/C 04577. Simultaneously the sample was treated with ultra sounds for 10 min.
After separation the layers obtained were analyzed chromatographically.
The GC analyses of the extracts were carried out according to the Polish Standard
PN-89/ C-04577 using gas chromatograph N-504 equipped with NUCOL capillary
column, 30 m, 0.25 μm at 60 C. Isotherm was 8 min, temperature increment ranged
between 5 C/min to 220 C, detector FID. The chromatograph was coupled with
computer registration and data processing system KSPD Metroster. In the case of
doubtful results and very small amounts of analytes the analyzes were performer using
HPLC method. A column 4 mm was applied and phase C18 of Knauer company in
isocratic conditions using eluent composed of 20% water and 80% methanol, detec-
tor UV, 254 nm, flow rate 1 cm3.
Nitrogen in water
After taking the samples they were put into the glass bottles and fixed by acidi-
fying with HCl to pH 1–2 and cooled down to temperature about 5 °C. The sam-
ples were then delivered to the laboratory. Analyses of nitrate nitrogen were car-
ried out using the colorimetric method while the nitrite nitrogen was determined
by the molecular absorption spectroscopy according to (PSa) and (PSb), respec-
tively.
Analytical methods 29
Airborne asbestos
The air samples were collected according to adapted Polish Standard (PS 1984) and
(Božek et al. 2016) using Quick Take 30 aspirator with an electronic flow control ad-
justment at the flow rate of 16.0 dm3/min and with 110 minutes sampling time applied.
The air stream was filtered on Sartorius cellulose nitrate membrane filters type 113,
with 25 mm diameter and 0.8 µm pores. After sampling the filters were protected in
boxes and delivered to the laboratory.
Prior to the microscopic examinations the filters were treated with diethyl
oxalate/dimethyl phthalate balsam in order to make them transparent. The fibrous
pollutants were identified and counted using the phase-contrast optical microscopy
PCOM, according to (PS 1988). The fiber counts from the measurements composed
a basis for further health risk assessment.
5. Occupational risk
posed by soil contaminants
5.1. Background
The case concerns estimation of the health risk in the occupational scenario on
a delimitated property used by engineers and other skilled workers employed as rail-
way carriage servicemen. The estimation comprises the following elements:
 assessment of ground contamination data,
 toxicological assessment of the identified anthropogenic pollutants,
 identification of the environmental hazard,
 exposure assessment in the occupational scenario,
 estimation of dose–response relation,
 risk characterization,
 uncertainty analysis.
Assessment of the health risk is a procedure within a scope of the environ-
mental risk assessment. Estimation of the health risk comprises qualitative and
quantitative assessment of the humans exposure to environmental contamination.
On this basis probability of manifestation of adverse health effects in a population
is determined.
In the procedure of occupational health risk assessment an exposure to upper layer
of the polluted soil was taken into account. Inhalation route of exposure was not con-
sidered because there were no circumstances for the presence of harmful anthropo-
genic substances in the air in significant concentrations. Ground waters had not been
taken into consideration, as well, for in the assumed scenarios no contact of the station
staff occurs with this exposure source.
The scope of the evaluation reflects the premises characteristics, use regime, type
of contamination and quality of analytical data. Risk assessment has been carried out
based on the US Environmental Protection Agency (US EPA) published in the docu-
ment Risk Assessment Guidance for Superfund. The latest toxicological data and pro-
cedures of risk assessment have been applied, as well. The applied methodology of the
32 Chapter 5
environmental risk estimation on the contaminated area is based on guidelines pub-

lished in the frame of American governmental project “Superfund” (EPA 1980).
Guidelines developed by Agency for Toxic Substances and Disease Registry were
taken into account, as well (ATSDR 2005).
In the considerations related to the exposure, legislation in force in Poland was taken
into account which relates to soils, ground waters and all kind of the environmental
pollution (ME 2002, ME 2008).
5.2. The site characterization
The considered facility is a delimitated property which is a part of a bigger com-

plete service infrastructure. It has a shape of slightly bent Wedge about 650 meters
long and 80 m wide (at its widest points). It is fitted with infrastructure intended for
railway carriage service. Figure 4 presents aerial view of the station with the indicated
ground and water sampling spots. In total 8 soil sampling points and 4 water sampling
points were installed. There are railway tracks, service hall, communication tracks and
other devices in the area.
Fig. 4. Aerial view of the facility with the indicated ground

and water sampling spots
Access to the area was provided for the regular staff and subcontractors. Profes-
sional activities connected with the rolling stock service and particularly with inspec-
Occupational risk posed by soil contaminants 33
tion of the train chassis are carried out irregularly, in periods determined by railway
accessibility. Exposure of the staff to the contaminants present in this area is a conse-
quence of a contact with the soil.
The geomorphology of the soils is unknown. Thus, it was not possible to de-
termine hazards posed by the contaminants migration from the Surface of the con-
sidered area to water bearing levels. The detected pollutants are of anthropogenic
origin.
5.3. Starting data
In the assessment procedure the pollutants have been taken into account which
most probably are present in the soil. They were identified based on the history and
features of the area which in the past was and still is used by entities related to rail-
ways. The following contaminants have been detected in the soil: arsenic, barium,
cadmium, cobalt, chromium, copper, molybdenum, nickel, lead, tin, zinc, mercury,
gasolines (hydrocarbons C6–C12), mineral oil, (hydrocarbons C12–C35), benzene,
ethylbenzene, toluene, styrene, m-, p-, o-xylene, naphthalene, phenanthrene, anthracene,
fluoranthene, chrysene, benzo(a)anthracene, benzo(a)pyrene, benzo(a)fluoranthene,
benzo(g,h,i)perylene.
Table 2 presents analyses of the soil samples collected from 8 sites from different
depths in the range between 0.0–0.3 m do 3.1–3.6 m.
Analyses of phenols showed minimum concentrations of monochlorophenol, di-
chlorophenols, trichlorophenols, tetrachlorophenols and pentachlorophenols in the
soil. None of the concentrations exceeds 0,1 mg/kg.
It should be noted that in the environment al analytics differentiation among
chemical forms of the same element is often neglected. From the point of view of the
environmental health risk assessment such proceedings are a drawback which makes it
impossible to estimate health risk precisely. In the case of chromium, for instance,
absence of speciation analysis distinguishing Cr(0), Cr(II) and Cr(VI) should be quali-
fied as a serious mistake. This is due to drastic differences in toxicity of these three
chromium forms. In such a case a conservative approach to risk assessment should be
applied which legitimates use of Cr(VI) toxic values, that is the most harmful chemi-
cal form of this element.
Due to the lack of the speciation analysis of the metal forms in the environment
the conservative approach was applied in this work. As a result certain overesti-
mation of the calculated risk may be expected. Until the risk values are acceptable
no repeated calculations and iteration are necessary to approach more real values
of the risk.
34 Chapter 5
Table 2. Analyses of the soil with respect of metals and hydrocarbons

concentration (gasolines, mineral oils, BTEX, PAH) (PIG 2016)
Sample No. 01 02 03 04 05 06 07 08
Dry mass 91.9 97 91.1 95.8 91.2 94.4 89.9 92.2
Metals
Arsenic (As) 2.62 <2 2.59 2.25 2.33 <2 2.76 <2
Barium (Ba) 53.4 <20 44.5 <20 40.2 <20 40.6 <20
Cadmium (Cd) <0.25 <0.25 0.333 <0.25 <0.25 <0.25 <0.25 <0.25
Cobalt (Co) 2.72 <2 <2 <2 2.1 <2 <2 <2
Chromium (Cr) 9 <5 7.87 <5 7.06 <5 6.52 <5
Copper (Cu) 19.6 <2 11.1 2.57 16.3 <2 7.81 <2
Molybdenum (Mo) <1 <1 <1 <1 <1 <1 <1 <1
Nickel (Ni) 6.02 1.1 3.92 1.48 3.81 <1 2.77 1.18
Lead (Pb) 21.6 <2 23.3 4.18 18.4 2.74 17.7 2.08
Tin (Sn) 5.79 <1 <1 <1 1.38 <1 <1 <1
Zinc (Zn) 85 <10 81.1 <10 52.2 <10 43.9 <10
Mercury (Hg) 0.0334 <0.0050 0.0583 0.0151 0.0404 0.0089 0.0361 0.0195
Aggregated parameters
Gasolines, total
(hydrocarb. C6–C12) <0.8 <0.8 <0.8 <0.8 <0.8 <0.8 <0.8 <0.8
Mineral oil
(hydrocarb. C12–C35) 15 <6 10 <6 12 <6 <6 <6
Volatile aromatic hydrocarbons (BTEX)
Benzene <0.01 <0.01 <0.01 <0.01
Ethylbenzene <0.01 <0.01 <0.01 <0.01
Toluene <0.01 <0.01 <0.01 <0.01
Styrene <0.01 <0.01 <0.01 <0.01
m-, p-, o-xylene <0.03 <0.03 <0.03 <0.03
BTEX, total <0.07 <0.07 <0.07 <0.07
Polyaromatic hydrocarbons (PAH)
Naphthalene 0.007 <0.005 <0.005 <0.005 0.006 <0.005 0.01 <0.005
Fenantrene 0.063 <0.005 0.032 0.014 0.059 <0.005 0.022 <0.005
Anthracene 0.026 <0.005 0.015 0.007 0.023 <0.005 0.012 <0.005
Fluoranthene 0.181 0.007 0.1 0.032 0.17 0.01 0.064 <0.005
Chrysene 0.108 <0.005 0.069 0.018 0.104 0.006 0.055 <0.005
Benzo(a)anthracene 0.092 <0.005 0.057 0.015 0.087 <0.005 0.038 <0.005
Benzo(a)pyrene 0.122 <0.005 0.07 0.019 0.109 0.006 0.051 <0.005
Benzo(a)fluoranthene 0.03 <0.005 0.017 <0.005 0.027 <0.005 0.011 <0.005
Benzo(g,h,i)perylene 0.1 <0.005 0.055 0.015 0.086 <0.005 0.037 <0.005
9 PAH, total 0.729 <0.045 0.415 0.12 0.671 <0.045 0.3 <0.045
Sample No 09 10 11 12 13 14 15 16
Dry mass 93.4 91.1 88.9 90.8 91.1 97.6 92.9 90.5
Metals
Arsenic (As) 3.59 2.64 2.51 2.33 2.88 <2 3.87 4.25
Barium (Ba) 56.8 52.4 42 26.6 39.6 <20 64.9 73
Cadmium (Cd) <0.25 <0.25 <0.25 <0.25 <0.25 <0.25 0.267 0.274
Cobalt (Co) <2 3.72 2.27 2.5 2.53 <2 3.11 3.2
Chromium (Cr) 5.79 14.9 9.47 9.9 12.9 <5 11.7 10.7
Copper (Cu) 16.5 14 12.9 5.79 6.39 <2 40.1 55.3
Molybdenum (Mo) <1 <1 <1 <1 <1 <1 <1 <1
Nickel (Ni) 3.43 8.03 6.93 5.33 5.71 1.73 8.14 8.26
Lead (Pb) 17.1 14 17.4 6.35 8.65 <2 84.6 87
Tin (Sn) 1.46 <1 1.1 <1 <1 <1 9.47 17.8
Zinc (Zn) 45.3 35.9 60.8 30.9 25.3 <10 83.3 82.9
Mercury (Hg) 0.049 0.031 0.054 0.047 0.037 0.006 0.048 0.048
Aggregated parameters
Gasolines, total
(hydrocarb. C6–C12) <0.8 <0.8 <0.8 <0.8 <0.8 <0.8 <0.8 <0.8
Mineral oil
(hydrocarb. C12–C35) 13 13 110 25 8.7 <6 140 46
Benzene <0.01 <0.01 <0.01 <0.01
Ethylbenzene <0.01 <0.01 <0.01 <0.01
Toluene <0.01 <0.01 <0.01 <0.01
Styrene <0.01 <0.01 <0.01 <0.01
m-, p-, o-xylene <0.03 <0.03 <0.03 <0.03
BTEX, total <0.07 <0.07 <0.07 <0.07
Polyaromatic hydrocarbons (PAH)
Naphthalene 0.008 0.02 0.013 <0.005 <0.005 <0.005 0.039 0.02
Fenantrene 0.085 0.517 0.089 0.042 0.008 <0.005 0.597 0.359
Anthracene 0.039 0.138 0.274 0.015 <0.005 <0.005 0.132 0.084
Fluoranthene 0.227 0.873 0.329 0.078 0.024 <0.005 1.27 0.787
Chrysene 0.143 0.427 0.316 0.042 0.016 <0.005 0.613 0.4
Benzo(a)anthracene 0.117 0.407 0.189 0.042 0.013 <0.005 0.497 0.323
Benzo(a)pyrene 0.14 0.441 0.314 0.05 0.016 <0.005 0.542 0.366
Benzo(a)fluoranthene 0.04 0.105 0.084 0.012 <0.005 <0.005 0.134 0.088
Benzo(g,h,i)perylene 0.104 0.286 0.144 0.034 0.017 <0.005 0.476 0.237
PAH, total 0.904 3.21 1.75 0.313 0.094 <0.045 4.3 2.66
36 Chapter 5
5.4. Hazard identification and toxicity assessment
Hazard identification was performer based on comparison soil chemical analyses,

toxicological properties of the contaminants and environment purity standards. The
pollution was identified in diverse soil layers. The contaminants found are classified
as xenobiotics potentially harmful to humans. Contamination concentrations were
compared to the soil quality standards classified to areas of C purity which are in-
tended for industrial activity, as well as to natural concentrations of impurities char-
acteristic for agricultural grounds.
In Table 3 threshold values of contaminants are given according to the decree of
Ministry of Environment dated September 9-th, 2002 concerning purity standards
for C group of grounds, that is industrial, mining and communication areas.
Comparison of the analyses of soil samples collected from the concerned area with
the standards of the Ministry of Environment leads to the conclusion that the occupa-
tional hazard posed by the exposure to the soil should not be a reason for major con-
cern. Recommended threshold concentrations for industrial areas are higher than the
real contents of the individual contaminants in the examined soil (Table 3).
Table 3. Purity standards for C group soils [mg/kg d.m.]*
Depth [m b.g.l.]**
>15 0–2 2–15 2–15
Contamination water permeability of soil [m/s]
below up to below
–7 –7
1  10 1  10
1 2 3 4 5
Arsenic 55 60 25 100
Barium 650 1000 300 3000
Chromium 380 500 150 800
Tin 300 350 40 300
Zinc 720 1000 300 3 000
Cadmium 10 15 6 20
Cobalt 120 200 50 300
Copper 200 600 200 1000
Molybdenum 210 250 30 200
Nickel 210 300 70 500
Lead 200 600 200 1000
Mercury 10 30 4 50
Cyanides (free) 12 40 5 100
Cyanides (complex compounds) 12 40 5 500
Gasoline (C6-12) – total 750 500 50 750
1 2 3 4 5
Mineral oils (C12-C35) 3000 3000 1000 3000
Benzene 50 100 3 150
Ethylbenzene 150 200 10 250
Toluene 150 200 5 230
Xylene 75 100 5 150
Styrene 100 60 2 100
Total aromatic hydrocarbons 150 200 10 250
Naphthalene 40 50 10 40
Fenantrene 40 50 10 40
Anthracene 40 50 10 40
Fluoranthene 40 50 10 40
Chrysene 40 50 10 40
Benzo(a)anthracene 40 50 10 40
Benzo(a)pyrene 40 50 5 40
Benzo(a)fluoranthene 40 50 5 40
Benzo(ghi)perylene 40 50 5 100
PAH (total) 200 250 20 200
Aliphatic chlorinated hydrocarbons
10 5 1 20
(volatile)
* [mg/kg d.m.] – mg/kg of dry matter,
** [m b.g.l.] – m below the ground level.
Also natural heavy metals levels in the soil are in most cases higher than those in
the soil collected from the railway station area concerned. Average contents of iron
and manganese, for instance, in samples taken in Borzęcin county in Małopolska re-
gion amounts to 10.8 and 0.30 g /g d.m., respectively. In samples taken from the depth
40–50 cm the concentrations were 11.4 and 0.30 g/kg d.m. Average contents of heavy
metals within 0-10 cm layer amounts to: 0.35 mg Cd; 19.9 mg Cr; 8.2 mg Cu; 10.2 mg
Ni; 18.1 mg Pb and 55.3 mg Zn/kg/ d.m. In the 40–50 cm layer the following concen-
trations were found: 0.13 mg Cd; 16.9 mg Cr; 5.1 mg Cu; 10.9 mg Ni; 7.3 mg Pb and
32.7 mg Zn/kg d.m.
In the samples taken from 0–10 cm depth the contents of Cd and Pb was 2.5 times
higher than these from 40–50 cm. In the case of Zn and Cu it was 1.7 times higher and
in case Cr 1.2 times higher. Only in the case of Ni the contents was similar in both soil
layers. As a background heavy metals concentrations reported by Kabata-Pendias et
al. (1993) were taken into account, that is 50 mg Zn, 0.3 mg Cd, 30 mg Pb, 15 mg Cu,
10 mg Ni and 20 mg Cr/kg d.m. (Czech et al. 2014).
Table 4 shows threshold contents of trace metals (mg/kg) in surface layer of soils
(0–20 cm), corresponding to different contamination levels, according to guidelines of
Institute of Soil Science and Plant Cultivation (IUNG). The values given relate to
three soil standard purity groups (A, B and C) which take into account different physi-
cal chemical and morphological properties of the soils (light, heavy soils, pH, clay
content, etc.) (IUNG 1993, Kabata-Pendias 1993, Kabata-Pendias and Piotrowska
38 Chapter 5
1995). As can be seen from the table, apart from zinc, no any case of heavy metals
exceedance in relation to the IUNG standards on the considered service station area
was found.
Table 4. Limit values of trace metals in surface soil layer (0–20 cm) [mg/kg]
Contaminant Soil group Concentration

A 30
Pb B 50
C 70
A 50
Zn B 70
C 100
A 15
Cu B 25
C 40
A 10
Ni B 25
C 50
A 0.3
Cd B 0.5
C 1.0
However by using the sewages for fertilization, permissible concentration of heavy

metals in 0–30 cm soil layer must not exceed values given in Ministry Decree (Dz.U.
2006), which are presented in Table 5.
Table 5. Permissible contents of heavy metals 0–30 cm soil layer [mg/kg d.m.]
Concentration
Metal
very light light medium heavy heavy
Lead (Pb) 20 40 60 80
Cadmium (Cd) 0.5 1 2 3
mercury (Hg) 0.7 0.8 1.2 1.5
Nickel (Ni) 10 20 35 50
Zinc (Zn) 60 80 120 180
Copper (Cu) 20 25 50 75
Chromium (Cr) 30 50 75 100
Despite of relatively low environment contamination it is not known if a real

health risk faced by the service station staff is acceptable or not. Soil pollutants found
in the area are not inert to the exposed people and an answer to the question whether
the real occupational health risk exceeds acceptable level is not known until a relevant
risk assessment procedure is made.
5.5. Toxicity profiles of the studied contaminants
Pollutants found on the railway service station show different health effects on
humans and animals. From among these effects toxic as well as carcinogenic influ-
ences should be mentioned. The toxic substances comply with the threshold theory
while the latter with linear theory. Probability of adverse health effects manifestation
depends on the exposition to the contamination which is affected by the environment
contamination level and exposure scenario.
The presented below synthetic toxicity profiles of individual contaminants cover
all examined pollutants from metal group, aromatic hydrocarbons, polycyclic aromatic
hydrocarbons, and chlorophenols. the data were extracted from different sources,
mainly from Integrated Risk Information System (IRIS) and Agency for Toxic Sub-
stances and Disease Registry (ASDR) databases. These data describe potential adverse
health effects posed by the exposure to harmful substances and maximum permissible
occupational concentrations published in the ordinance of Minister of Labor and So-
cial Care dated June, 6-th 2014 on maximum permissible concentration and intensity
of harmful factors in the work environment in accordance with national limit values
(Dz.U. 2014). Table 6 presents toxic profiles of the pollutants and maximum permis-
sible concentrations MPC [mg/m3] in the workplace.
Table 6. Toxicity profiles of individual pollutants

and maximum permissible concentrations MPC [mg/m3] in the workplace
Hazardous
Toxicity profile MPC
factor
1 2 3
Arsenic compounds enter the organism from digestive tracts, through skin
and respiratory tracts. Inorganic III-valent arsenic compounds which are
easily water-soluble assimilate from the digestive tracts in 45–95%, while
the sparingly soluble (arsenic sulfide) are absorbed to a negligible extent.
Arsenic compounds may block enzymes activity, mostly by causing distur-
bances in Krebs cycle. Inorganic arsenic compounds are more harmful than
the organic ones and from among these inorganic the most toxic is III-valent
arsenic, for instance arsenic trihydride (AsH3) and arsenic trioxide (As2O3).
Arsenic 0.01
Symptoms of the gastro-intestinal catarrh are observed leading to water-
electrolyte disorders and distress. At the same time rapid fall in blood pres-
sure may occur. Anemia, leucopenia and nervous system disorders can be
observed, as well. A dose 70–300 mg of arsenic trihydride is considered
a lethal dose a lethal dose a lethal dose an average lethal dose for humans.
Inorganic arsenic compounds exhibit carcinogenic effects in humans. Per-
manent inhalation exposure considerably rises risk of lung cancer, while
after oral exposure to arsenic compounds skin cancer may occur.
40 Chapter 5
1 2 3
Barium and its soluble compounds influences toxically the cardiovascular
system causing blood overpressure and cardiac arrhythmia. Poisoning with
barium compounds involves acute gastro-intestinal disorders, muscular
weaknesses and muscle paralysis. As a result of acute barium compounds
Barium 0.5
poisoning kidney failure, rhabdomyolysis, dysphagia and arterial hyperten-
sion may occur. As a consequence of respiratory muscle paralysis breath-
holding and death may occur. Barium and its soluble compounds are not
mutagenic, genotoxic and nor carcinogenic (Surgiewicz 2011).
Cadmium is absorbed from respiratory and digestive systems. An intensi-
fied excretion of low-molecular proteins in urine is a critical effect of cad-
Cadmium mium in the body. In the case of respiratory tracts exposure carcinogenic 0.01
effects may be demonstrated. Cadmium and its inorganic compounds are
classified as probably carcinogenic to humans. (Jakubowski 2012).
Exposure to cobalt in the occupational conditions proceeds mainly
through dusts and smokes. Chronic non-occupational poisoning can be a
result of consumption of larger amount of beer containing cobalt sulfate as
an additive. Such poisoning is demonstrated by myocardial damage, in-
crease in the amount of red blood corpuscles and disorders of thyroid me-
Cobalt tabolism. People exposed to cobalt by respiratory tracts and dermal contact 0.02
demonstrate allergy and weak irritation. Respiratory tracts are a critical
system affected by cobalt. It is manifested by asthma and allergic diseases,
functional disorders may also occur resulting in impairment of respiratory
fitness. IARC classified cobalt and its compounds to group 2B (Possibly
carcinogenic to humans) (Sapota 2011).
Direct contact with chromium compounds results in irritation and slow-
healing skin ulcers. Chromium(VI) compounds contribute significantly to
the development of contact dermatitis. Chronic exposition to chromium(VI)
increases risk of cancer lung development. Apart from their carcinogenic
0.5
effects, the Cr(VI) compounds can irritate respiratory tracts which leads to
for Cr(0),
damages of nasal cavity tissues, perforation of nasal septum, ulcers and nose
Cr(II) and
Chromium bleeds. Papilloma of the upper respiratory tracts is possible, as well. Also
Cr(III),
renal damage is reported among workers exposed to chromium(VI) which
0.1
manifests by an increase of β microglobuline in urine and by renal tubes
for Cr(VI)
necrosis. Kidney exposition to chromium compounds results in an increase
in reactive intermediate compounds that manifests in oxidative kidney dam-
age. Chromium(III) is considered thousand times less toxic than chromium
III (Surgiewicz 2009).
Ingestion of copper leads to disturbances of alimentary tract and liver.
Based on epidemiological experiments it was proved that expose to copper
increases mortality risk caused by cerebral vessel diseases and Parkinson
disease. It promotes the development of atherosclerosis, as well. In respect
Copper 0.2
of acute toxicity the copper compounds were classified to harmful sub-
stances. Cu and its compounds are not classified In term of carcinogenicity,
however it was proved that they can demonstrate embryotoxic, fetotoxic and
teratogenic effects (Starek 2011).
1 2 3
So far, molybdenum has not been classified as a dangerous substance. In
a pulverized form it is highly flammable, as a solid it is harmless. Molybde-
num dust can be sparsely irritating. It can cause tearing, pain and eye red-
Molybdenum 4
ness, cough and shortness of breath. Chronic exposure to high molybdenum
concentrations can result in pneumoconiosis, anemia, uric acid increase in
blood, gout attacks, hypothyreosis and liver damages (Gawęda 2014).
Among those exposed to nickel in volatile form (vapors, aerosols, dust)
increased risk of lung and upper respiratory tract cancer has been found.
Asthma, pneumoconiosis, chronic rhino-conjunctivitis with perforation of
nasal septum and loss of smell. Chronic toxic effects of nickel can proceed
Nickel 0.25
as a result of free oxygen radicals formation. Nickel is capable of induction
of numerous processes responsible for oncogenesis. chronic exposure to
high nickel doses causes weakening the innate immunity. Also toxic effects
of Ni on NK lymphocytes is reported which help fight virus infections.
In the case of exposure to lead the critical systems in adults are hematopoietic
system, cardio-vascular system, nervous system and kidneys. In children the
critical is the nervous system. Early consequences of lead in these systems
are demonstrated in adults at the lead concentration in blood amounts to
Lead 0.05
about 300 μg/L or even below this value. In children lead is a non-threshold
factor in respect to central nervous system. Lead is recognized by IARC as
a factor with sufficient evidence of carcinogenicity in experimental animals and
strong evidence for carcinogenesis in humans (group 2A) (Jakubowski 2014).
Inorganic tin compounds, similarly to lead, interfere processes of hem
biosynthesis that leads to anemia. The organic compounds hinder cellular
respiration processes. Tin compounds used in fungicides interfere calcium,
2 inhaled
Tin magnesium, potassium and sodium ions transport through mitochondrial
fraction
membranes, thus they block ATPaz activity in the brain. Tin compounds
decrease concentration of catecholamines in the brain and adrenals. Tin is
also irritating to skin and respiratory tracts.
Zinc-caused poisoning manifests through compromised immune response,
reduction of HDL cholesterol fraction, decreased level of copper in blood. Acute
1 (ZnCl2)
Zinc poisoning with zinc reflects in vomiting, upper abdominal pain, fatigue and
5 (ZnO)
lethargy. Zinc chloride (ZnCl2) irritates skin, mucous membranes and conjunc-
tiva of the eye. In higher concentrations it is a cause of burnings (Seńczuk 2006).
Mercury poses a hazard to living organisms even in low concentrations. Or-
ganic forms of mercury are usually more harmful (even 10 times) than the inor-
ganic ones. The concentration 5 μg/l already causes toxic effects in water envi-
ronment. Mercury compounds may interfere majority of enzymatic reactions
because they react with peptides containing sulfhydryl groups. The highest
mercury concentration occurs in kidneys, while brain is the susceptible to dam-
Mercury ages. Methylmercury concentration in the brain may reach a level 5 times higher 0.02
than in blood.
Mercury vapors affect toxically the lungs, causing as a result respiratory insuf-
ficiency and death. Chronic exposure to low mercury vapors concentration may
cause damage to the central nervous system with fatigue symptoms, memory
disorders, changing moods, headache. pain in extremity, inflammation of the
gums and mucous membrane and others (Seńczuk 2006).
42 Chapter 5
1 2 3
Exposure to benzene may cause leucosis in affected humans. Different
types of the leucosis is observed such as acute and chronic myelogenous
leukemia, chronic lymphocytic leukemia and multiple myeloma. In experi-
mental animals, apart from leukemia, Zymbal’s gland tumor, cancer of the
stomatitis and nasal cavity, cancer of foreskin gland and ovaries are re-
ported.
Benzene is not a mutagenic factor in in vitro assays. However this com-
pound or its metabolites may induce chromosome aberrations, cause in-
Benzene crease in the frequency of micronuclei or sister chromatids exchange. Ben- 1.6
zene injected to peritoneal cavity may cause morphological defects of
sperm. Genotoxicity of benzene was reported in humans exposed occupa-
tionally. Benzene is not a teratogen to animals; its embryotoxicity and fe-
tototoxicity was observed only when the concentrations were toxic also for
mothers. Results of numerous epidemiological investigations proved that
benzene is a carcinogenic factor to humans hematopoietic and lymphoid
systems. IARC qualified benzene to group l, which means it is considered as
carcinogenic factor to humans (Lebrecht et al. 2003).
Ethylbenzene vapours at higher concentrations can irritate eyes, throat and
humans upper respiratory passages. They also may depress the central nerv-
ous system. Ethylbenzene may damage liver and kidneys in persons ex-
Ethylbenzene 200
posed., however no mutagenic and teratogenic effects have been proved. On
the other side in animals evident carcinogenic effects have been demon-
strated (Soćko and Czerczak 2010).
Toluene may cause acute neurologic effects including euphoria and sub-
sequent depression. Also metabolic abnormalities are associated to acute
Toluene toluene intoxication. It has been reported that rhabdomyolysis and acute 100
hepatorenal injury could be hallmarks of the condition, and could constitute
risk factors for poor outcomes (Camara-Lemarroy et al. 2015).
Toxic activity of styrene is manifested by eye, nose and throat membranes
irritation. Also impairment of the central nervous system in form of neuro-
behavioral effects as well as hearing and vision impairments may occur. In
workers chronically exposed to styrene clinical signs of haematological
changes are observed. Functional disorders of liver, endocrine system dam-
Styrene 50
ages and immunological problems were noticed, as well. Styrene has geno-
toxic activity which is manifested by clastogenic and chromosome aberra-
tions caused by the formation of DNA adducts. According to IARC there are
no sufficient proofs of carcinogenic effects of styrene in humans (Starek
2012).
Based on the results of acute and chronic toxicity assays in animals it was
m-, p-,
found that xylene has relatively weak adverse health effects and is not clas- 100
o-xylene
sified as mutagenic or carcinogenic factor (Ligocka 2007).
Naphthalene is a carcinogenic substance, dangerous to the environment.
Limited proofs of its carcinogenicity have been found. It is harmful after
Naphthalene 20
After being ingested. Very toxic to aquatic life. Naphthalene may cause
long-term adverse effects in the aquatic environment.
1 2 3
Polycyclic Epidemiological studies made on workers exposed to polycyclic aromatic
aromatic hydrocarbons, benzo(a)pyrene among others, demonstrated a clear relation-
hydrocarbons ship between exposure to these mixtures and rise in carcinogenic risk. Epi-
(PAHs) demiological investigations show a relationship between occupational expo-
sure to PAHs and excess cancer incidents in workers. IARC considered jobs
in such industries as cox, steel mill, rubber, aluminum industries to be the
factor favouring development of cancer (IARC, 1989). In Poland from 0.002
among 1042 cases of occupational cancers observed in men (average age (sum)
55 years), in the years 1971–1994, 673 cancers were located in the upper
respiratory tracts. Of those, 29% cases are cancers caused by exposure to
PAHs. Benzo(a)pyrene is a chemical carcinogen classified to indirect car-
cinogens (pre-carcinogen) which, to cause a result, has to undergo a me-
tabolism process towards an active form of electrophilic properties (Sapota
2002).
In Table 7 basic toxic data of the analyzed pollutants are given along with car-
cinogenicity classification that are extracted from IRIS EPA and ATSDR data-
bases.
Without a doubt, three pollutants are classified as carcinogenic to humans
(group A). One is in the group B1, and the next 7 are in group B2. One pollutant is in
group C, while the remaining 15 are in group D (not classifiable as to human carcino-
genicity). This classification refers to oral exposure. Naphthalene is in group C and is
not harmful in the oral exposure but no information is available concerning its inhala-
tion exposure.
Lack of figures concerning cancer slope factors of some pollutants makes it impos-
sible to determine the health risk quantitatively. Descriptions available in EPA data-
base enable to estimate the risk only qualitatively. In the case of the pollutants found
in the ground the risk should not be of significance particularly when oral expose route
is taken into account and the concentrations are very low.
In the case of three pollutants: arsenic, benzene and benzo(a)pyrene their carcino-
genicity is obvious. In the database cancer slope factors of these pollutants are the
following: 0.002; 0.055 and 7.3 [(mg/k * d)–1], respectively, which are high.
Table 7. Toxic parameters of the pollutants (EPA 2011c, ATSDR, IARC

(International Agency for Research on Cancer), RAIS) – the data concern oral expose route
NOAEL/*LOAEL RfD SForal Carcinogenicity

Pollutant
mg/kg * d mg/kg * d (mg/kg * d)–1 group
1 2 3 4 5
Metals
Arsenic (As) 8  10–4 3  10–4 2  10–3 A
Barium (Ba) and comp. 2  10–1 D
Cadmium (Cd) 1  10–2 1  10–3 B1
44 Chapter 5
1 2 3 4 5
0.03
Cobalt (Co) 0.6 (ATSDR 2004) not class.
(Finley et al. 2012)
Chromium(III) (Cr(III)) 1.468E+03 1.5 D
Chromium(VI) (Cr(VI)) 2.5E+00 3  10–3 D
Copper (Cu) D
Molybdenum (Mo) *1.4  10–1 5  10–3 D
Nickel (Ni) soluble salts 2  10–2 B2
Lead (Pb and comp. *20 µg/kg * d **n/a B2
Tin(Sn) 63 D
Zinc (Zn) *0.91 3  10–1 D
Mercury (Hg) as HgCl2 *3.17  10–1 3  10–4 D
Benzene 4  10–3 5.5  10–2 A
Ethylbenzene 9.71  101 1  10–1 D
Toluene 223 8  10–2 D
Styrene 2.00  102 2  10–1 B2
m-, p-, o-xylene 1.79  102 2  10–1 D
Polycyclic aromatic hydrocarbons (PAH)
Naphthalene 7.1  101 2  10–2 C
Fenantrene – – D
Anthracene 1.000 103 3  10–1 D
Fluoranthene 1.25  102 4  10–2 D
Chrysene – – B2
Benzo(a)anthracene – – B2
Benzo(a)pyrene – 2  10–4 7.3 B2
Benzo(a)fluoranthene – – B2
Benzo(g,h,i)perylene – – D
The risk assessment was accomplished based on the guidelines of the American
governmental project “Superfund” (EPA 1980, 1989). Also guidelines developed by
Agency for Toxic Substances and Disease Registry (ATSDR 2005) were applied. For
the purpose of the assessment exposure scenarios for occupational activity was applied
and analytical data concerning soil pollution in the service station. The considerations
were carried out separately for the toxic and carcinogenic pollutants.
Toxic substances
It was assumed in this work that the toxic substances comply with the threshold
theory. According to this theory adverse health effect in the organism is manifested
if the threshold dose is exceeded. It was proved that living organisms developed
defensive mechanisms which cease working once the threshold dose has been ex-
ceeded. The dose is a distinctive feature for a toxic substance. Below the threshold
no adverse health effects are observed thanks to the defensive mechanisms.
For determination of non-carcinogenic effects, that is toxic, an approach involving
reference dose RfD is applied. Reference dose is derived from maximum concentration
or dose with no observed adverse health effect (No Observed Adverse Effect Level
– NOAEL). Similarly, the no observed adverse effect level (NOAEL) denotes the level
of exposure of an organism, at which there is no biologically or statistically significant
increase in the frequency or severity of any adverse effects in the exposed population
when compared to its appropriate control.
Value of reference dose is derived from NOAEL using modifying factor (MF) and
uncertainty factor (UF), taking into account extrapolation errors of experimental doses
and safety margin. Reference dose or reference concentration are basic indicators of
toxicity applied for determination of hazard quotients resulted from exposure to
chemical pollutants.
Carcinogenic substances
For carcinogenic substances linear response theory was applied assuming that
there is no safe threshold dose and each dose, even the smallest one, may cause an
adverse health effect.
For this type of the harmful substances cancer slope factor CSF is a measure of
carcinogenicity that is applied for the cancer health risk calculations. CSFs expressed
as (mg/(kg · d))–1 are published in databases which are available on EPA and ATSDR
websites, among others.
The assumption has been made that the exposure to the pollutants takes place in
the course of service works at railway units that are associated with unavoidable inci-
dental or intentional contact with the soil. Taking into account probable exposure sce-
narios, contact with ground waters was excluded. Also inhalation exposure route was
considered to be irrelevant.
Basic expose route is incidental soil ingestion occurring during the service and
maintenance works, contact of hands with the face and mouth regions. Food con-
sumption at the work stand can also contribute to the ingestion of certain amount of
the soil. EPA standards (EPA 2009, EPA 2011b) were applied for determination of
accidental ingested doses of soil.
Literature on behaviors leading to the increase of exposure by the incidental soil
ingestion is very extensive. Majority of reports relates to children. Generally the in-
gestion rates decrease with the age. For adults the dose is dropping to minimum. Chil-
dren of the age below 24 (Tulve et al. 2002) insert statistically different objects and
their fingers as many as times 81, while the older ones repeat such an operation not
more frequently as 42 times.
46 Chapter 5
It is understandable that the frequency of touching the mouth and placing different
objects in it is significantly less in group of adults. Experimental data confirm that the
behaviour of touching the mouth region repeats 3.9 times per hour while mouthing
occurs 1.6 times per hour. Oral soil exposure model resulting from such a behaviour is
presented in Fig. 5.
Fig. 5. Model of inadvertent ingestion exposure of hazardous substances in the soil

(Christopher et al. 2007)
Daily dose of the ingested soil in children ranges between 40 to 270 mg, while the
average dose amounts to 100 mg/d (EPA 1997). According to ATSDR (2005) a child
of 10 kg ingests about 200 mg of soil daily. When adult is concerned insufficient ob-
servations are available to determine precise data, nevertheless the maximum dose of
100 mg/d is applied and the average amounts to 50 mg/d (EPA 1997). The latter value
has been applied to estimate the health risk in this work.
The following assumptions and exposure scenarios were used in the calcula-
tions:
 exposure frequency for diverse staff groups:
– (A) 1 h/168h (0.05/8),
– (B) 0.5 h/40h (0.1/8),
– I 1 h/8h (1/8),
– (D) constant exposure within 8h/40h (8/8);
 exposure periods were applied for two extreme staff age groups: 4.4 years for
the age group 25–29 and 19.4 years for workers from the age group 60–64 years
(EPA 1997, Concha-Barrientos et al. 2004);
 model of occupational exposure by incidental soil ingestion by Christopher

et al. (2007) has been applied;
 incidental soil ingestion rate was applied according to ATSDR and EPA (Moya
2011; EPA 2011b) that is 100 mg/d;
 toxic measures for metals in inorganic form have been applied.
The following equation was applied for calculation of the chronic daily doses CDI
(Chronic Daily Intake) of individual pollutants (EPA 1991, Čáslavský et al. 2010):
s
CDI ING , i  cSi  IRING , S  FI   EF  ED  BW 1  AT 1  10  6 [mg  kg 1  d 1 ] (13)
S
where:
cSi [mg/kg] – average concentration of the i-component,
IRING, S [mg/d]– daily rate of accidental ingested soil – 100 (Moya 2011, EPA
2011b),
FI  0; 1 – fraction ingested during full-shift contact with the polluted soil in
the concerned area (0.5 applied (ATSDR 2005)),
s [h] – actual number of contact hours within one shift. Values on four
levels have been applied (0.05; 0.1; 1 and 8 h)
S [h] – duration of a standard shift (8),
EF [d/y] – exposure frequency (230),
ED [y] – exposure period – ED for two extreme staff age groups has been
applied: age group 25–29 years – ED = 4.4 years and age group
60–64 years – ED = 19.4 years (EPA 1997, Concha-Barrientos
et al. 2004),
BW [kg] – average body weight (80),
AT [d] – averaging time (time period during which the pollutants’ concen-
trations are considered as constant), for toxic effects equal to ex-
posure time, for carcinogenic equal to 25 550 (lifetime in d),
–6
1  10 – conversion factor [kg/mg].
In the case of carcinogenic exposure the so called Lifetime Average Daily Dose
LADD is calculated, in which case average life expectancy is used for averaging the
dose (70 years). The equation has the same form as the equation (1) with the exception
that the AT parameter is constant and amounts to 25 550 days.
Table 8 presents ingested chronic doses calculated according to the expression
(1) for all considered exposure scenarios, in mg per day and kg of body weight.
These doses were used for determination of dose–response relationship expressed
by hazard quotients HQ and hazard indices HI. A conservative approach to the
hazard and risk determination was applied, which means that some overestimation
of the obtained risk values is expected. Such attitude was aimed at the protection
of the health and safety of workers from the risks related to chemical agents at
work.
48 Chapter 5
Table 8. Daily doses in chronic toxic exposure (CDI) to individual pollutants

in scenarios A, B, C and D for extreme age groups of workers,
that is 25–29 and 60–65 years [mg/(kg * d)]
Doses in toxic exposure CDI

Pollutant age groups 25–29 years and 60–64 years
A B C D
Arsenic (As) 7.12E–09 1.42E–08 1.42E–07 1.14E–06
Barium (Ba) 1.18E–07 2.35E–07 2.35E–06 1.88E–05
Cadmium (Cd) 6.46E–10 1.29E–09 1.29E–08 1.03E–07
Cobalt (Co) 5.76E–09 1.15E–08 1.15E–07 9.22E–07
Chromium (Cr) 2.16E–08 4.33E–08 4.33E–07 3.46E–06
Copper (Cu) 4.02E–08 8.04E–08 8.04E–07 6.43E–06
Molybdenum (Mo) 2.46E–09 4.92E–09 4.92E–08 3.94E–07
Nickel (Ni) 1.25E–08 2.51E–08 2.51E–07 2.01E–06
Lead (Pb) 6.42E–08 1.28E–07 1.28E–06 1.03E–05
Tin (Sn) 6.83E–09 1.37E–08 1.37E–07 1.09E–06
Zinc (Zn) 1.47E–07 2.93E–07 2.93E–06 2.35E–05
Mercury (Hg) 1.10E–10 2.20E–10 2.20E–09 1.76E–08
Benzene 2.46E–11 4.92E–11 4.92E–10 3.94E–09
Ethylbenzene 2.46E–11 4.92E–11 4.92E–10 3.94E–09
Toluene 2.46E–11 4.92E–11 4.92E–10 3.94E–09
Styrene 2.46E–11 4.92E–11 4.92E–10 3.94E–09
m-, p-, o-xylene 7.38E–11 1.48E–10 1.48E–09 1.18E–08
Naphthalene 2.46E–11 4.92E–11 4.92E–10 3.94E–09
Fenantrene 2.95E–10 5.91E–10 5.91E–09 4.73E–08
Anthracene 1.72E–10 3.45E–10 3.45E–09 2.76E–08
Fluoranthene 7.38E–10 1.48E–09 1.48E–08 1.18E–07
Chrysene 3.20E–10 6.40E–10 6.40E–09 5.12E–08
Benzo(a)anthracene 3.45E–10 6.89E–10 6.89E–09 5.51E–08
Benzo(a)pyrene 4.18E–10 8.37E–10 8.37E–09 6.70E–08
Benzo(a)fluoranthene 9.85E–11 1.97E–10 1.97E–09 1.58E–08
Benzo(g,h,i)perylene 3.20E–10 6.40E–10 6.40E–09 5.12E–08
Table 9 shows the results of calculations of the doses in carcinogenic exposure

scenario, according to modified equation (1). The doses relate to all pollutants, how-
ever only these applying to carcinogenic pollutants were used to determine lifetime
cancer risk.
As can be seen from Tables 8 and 9, average pollutants’ doses in all expose
scenarios, both toxic and carcinogenic are very low. They are at the level of 10–11
– 10–7 mg/(kg * d). A question if they are dangerous for the workers can be answered
when the dose–response analysis is made. For this purpose hazard quotients and life-
time excess cancer risk must be calculated.
Table 9. Lifetime average daily doses in carcinogenic exposure (LADD)

of individual pollutants in scenarios A, B, C and D
for extreme age groups 25–29 years and 60–64 years [mg/(kg * d)]
Doses in toxic exposure CDI

Pollutant Age groups 25–29 years and 60–64 years
A B C D
Arsenic (As) 7.12E–09 1.42E–08 1.42E–07 1.14E–06
Barium (Ba) 1.18E–07 2.35E–07 2.35E–06 1.88E–05
Cadmium (Cd) 6.46E–10 1.29E–09 1.29E–08 1.03E–07
Cobalt (Co) 5.76E–09 1.15E–08 1.15E–07 9.22E–07
Chromium (Cr) 2.16E–08 4.33E–08 4.33E–07 3.46E–06
Copper (Cu) 4.02E–08 8.04E–08 8.04E–07 6.43E–06
Nickel (Ni) 1.25E–08 2.51E–08 2.51E–07 2.01E–06
Lead (Pb) 6.42E–08 1.28E–07 1.28E–06 1.03E–05
Tin (Sn) 6.83E–09 1.37E–08 1.37E–07 1.09E–06
Zinc (Zn) 1.47E–07 2.93E–07 2.93E–06 2.35E–05
Mercury (Hg) 1.10E–10 2.20E–10 2.20E–09 1.76E–08
Benzene 2.46E–11 4.92E–11 4.92E–10 3.94E–09
Toluene 2.46E–11 4.92E–11 4.92E–10 3.94E–09
Styrene 2.46E–11 4.92E–11 4.92E–10 3.94E–09
m-, p-, o-xylene 7.38E–11 1.48E–10 1.48E–09 1.18E–08
Fenantrene 2.95E–10 5.91E–10 5.91E–09 4.73E–08
Anthracene 1.72E–10 3.45E–10 3.45E–09 2.76E–08
Chrysene 3.20E–10 6.40E–10 6.40E–09 5.12E–08
Benzo(a)anthracene 3.45E–10 6.89E–10 6.89E–09 5.51E–08
Benzo(a)pyrene 4.18E–10 8.37E–10 8.37E–09 6.70E–08
Benzo(a)fluoranthene 9.85E–11 1.97E–10 1.97E–09 1.58E–08
Benzo(g,h,i)perylene 3.20E–10 6.40E–10 6.40E–09 5.12E–08
5.7. Determination of dose–response relation
Determination of dose–response relation enables to assess health hazard quantita-

tively. Unfortunately, toxic data of many substances remain still unknown. Their tox-
icity measures had not been determined yet, thus, to estimate level of hazard and
health risk posed by these substances, some simplifications and assumptions are nec-
essary. In many cases use of data characteristic for reference, equivalent substances is
advised.
50 Chapter 5
In the absence of the necessary data for carrying out the calculations values of
reference doses and cancer slope factors of the most toxic form of a substance is
applied.
In case metals concerned with in this work, all the necessary data needed for de-
termination of absorbed doses and all toxic indices are available. As regards hydrocar-
bons, reference doses are known only for naphthalene, anthracene and fluoranthene.
From among these pollutants only benzene and benzo(a)pyrene have proven carcino-
genic properties.
It should be noted, that kind and intensity of the negative health effects in humans
depend to a large extent on exposure route. Three-valent chromium compounds, for
instance, are not carcinogenic both in oral and inhalation exposure, while chromium(VI)
is a strong carcinogen in inhalation expose route. Besides, it is believed that the latter
form is thousand times more toxic than Cr(III). Chromium Cr(0) is not toxic.
The dose–response relation should be considered in two aspects: toxic and muta-
genic effects. Followed considerations and calculations are presented in respect to
both types of the health effects.
Toxic effects
Toxic substances, that is non-carcinogenic comply with the threshold theory in
their effects on humans and animals. In the case of such substances, reference doses
and reference concentrations (RfD and RfC) are applied to determine the health
hazard levels. RfD and RfC are derived from the so called “no-observed-adverse-
effect-level” (NOAEL), that is the highest threshold dose or concentration with no
observed negative health effects. Similarly the “lowest-observed-adverse-effect-
-level” (LOAEL) is defined as the lowest dose or concentration causing the negative
health effects.
Hazard Quotient HQ considered as a measure of non-carcinogenic hazard level
constitutes in fact a comparison of the absorbed dose CDI of a substance with its ref-
erence dose RfC. So, values of HQ are calculated from the following expression (EPA
1992):
HQ = CDI/RfD (14)
For the exposure to multiple hazardous substances Hazard Index HI is calculated
according to:
m
HI   HQ
i 1
i (15)
where HQi is a hazard quotient for the i-substance.

The calculated values of HQ and HI for the above described scenarios are given in
Table 10.
Table 10. Hazard quotients HQ and hazard indices HI

for the workers’ groups in the exposure scenarios A, B, C and D
Hazard Quotient HQi

Pollutant Workers’ age groups 25–29 years and 60–64 years
A B C D
Arsenic (As) 2.37E–05 4.75E–05 4.75E–04 3.80E–03
Barium (Ba) 5.88E–07 1.18E–06 1.18E–05 9.40E–05
Cadmium (Cd) 6.46E–07 1.29E–06 1.29E–05 1.03E–04
Cobalt (Co) 1.92E–07 3.84E–07 3.84E–06 3.07E–05
Chromium (Cr) 7.21E–06 1.44E–05 1.44E–04 1.15E–03
Copper (Cu) 0 0 0 0
Nickel (Ni) 6.27E–07 1.25E–06 1.25E–05 1.00E–04
Lead (Pb) – – – –
Tin (Sn) 2.34E–09 4.67E–09 4.67E–08 3.74E–07
Zinc (Zn) 4.89E–07 9.78E–07 9.78E–06 7.83E–05
Mercury (Hg) 3.67E–07 7.34E–07 7.34E–06 5.87E–05
Benzene 1.73E–03 3.46E–03 3.46E–02 2.77E–01
Toluene 3.08E–10 6.15E–10 6.15E–09 4.92E–08
Styrene 1.23E–10 2.46E–10 2.46E–09 1.97E–08
m-, p-, o-xylene 3.69E–10 7.38E–10 7.38E–09 5.91E–08
Fenantrene 0 0 0 0
Anthracene 5.74E–10 1.15E–09 1.15E–08 9.19E–08
Chrysene 0 0 0 0
Benzo(a)anthracene 0 0 0 0
Benzo(a)pyrene 0 0 0 0
Benzo(a)fluoranthene 0 0 0 0
Benzo(g,h,i)perylene 0 0 0 0
Hazard Index
1.76E–03 3.53E–03 3.53E–02 2.82E–01
HI = Σ HQi
* According to EPA data hazard level associated with the exposure to lead compounds is very low. Critical
effects appearing after the exposure to lead (alterations in certain enzymes level in blood, high blood pressure,
neurobehavioural problems in children) occur at as low exposure (expressed by Pb level in blood) that it is
impossible to make an accurate estimation of threshold values for this pollutant. Therefore determination of the
reference dose for lead cannot be established. Thus, hazard posed by the exposure to lead may be expressed in
purely descriptive manner based on morphological examinations of the exposed persons.
Carcinogenic effects
Carcinogenic substances comply with the linear theory. In the risk calculations
cancer slope factor is used which is determined In immunological studies and assays
52 Chapter 5
performed in animals, separately for each exposure route. In the followed calculations
oral exposure to contaminated soil was taken into account.
For carcinogenic effects the so called Excess Lifetime Cancer Risk ELCR occur-
ring when a population is exposed to these substances. For a single substance at a very
low concentration the following expression is valid:
ELCR = LADDCSF (16)
where:
ELCR – excess lifetime cancer risk,
CSF – cancer slope factor [(mg/(kg  d))–1],
LADD – chronic daily dose of a substance averaged over the lifetime 70 years
[mg/(kgd)].
General equation for whole concentration range is as follows:
ELCR = 1 – e–(LADDCSF). (17)
In case of multiple substances fund in the environment the so called total risk is
calculated as a sum of risks posed by individual pollutants:
m
ELCR t   ELCR
i 1
i
(18)
where:
ELCRt – total excess lifetime cancer risk,
ELCRi – the estimation of the risk posed by the i-substance.
In the specialist literature risk of 10–6 is considered as acceptable however this
value has not been codified. Depending on the profession performed the acceptable
risk may be established at different levels. In Table 11 results of risk calculations
ELCRi and ELCRt are given for exposure scenarios applied in this work.
Table 11. Excess risks for individual carcinogenic pollutants ELCRi

and total risks cancer ELCRt calculated for the applied occupational exposure scenarios
Excess lifetime cancer risk ELCRi
Pollutant Age group 25–29 years Age group 60–64 years
A B C D A B C D
Arsenic 8.95E–13 1.79E–12 1.79E–11 1.43E–10 3.95E–12 7.90E–12 7.90E–11 6.32E–10
Benzene 8.50E–14 1.70E–13 1.70E–12 1.36E–11 3.75E–13 7.50E–13 7.50E–12 6.00E–11
Benzo(a)pyrene 1.92E–10 3.84E–10 3.84E–09 3.07E–08 8.47E–10 1.69E–09 1.69E–08 1.35E–07
ELCRtot 1.93E–10 3.86E–10 3.86E–09 3.09E–08 8.51E–10 1.70E–09 1.70E–08 1.36E–07
It can be seen from the calculations that hazard index HI for all the scenarios
(A – 0.05/8; B – 0.1/8; C – 1/8 and C – 8/8) and workers’ age groups ranges between
1.76 * 10–3 and 0.282, while the excess carcinogenic risk ELCR is between 1.93 * 10–9
in scenario A, and 1.36 * 10–7 in scenario C. Figures 6 and 7 present graphical com-
parison of hazard indices and carcinogenic risks depending on the applied exposure
scenarios and workers’ age groups.
Fig. 6. Comparison of hazard indices HI Fig. 7. Comparison of carcinogenic risks ELCR

for exposure scenarios A, B, C and D for exposure scenarios A, B, C and D
(HI are the same for both age groups) for workers’ age groups
The calculated excess life time cancer risk ELCR in the workers group is very low.
It amounts to just 10–9–10–7. According to informally recognized standards, the un-
conditionally accepted health risk level is 1 * 10–6. We must be aware of the fact that
this is a stipulated, informally imposed, non-codified value which does not constitute
a legal standard. However it is commonly used by specialists dealing with the health
risk estimation.
Risk of 10–4 is considered as tolerable, while 10–3 is absolutely not acceptable and
in that case protective measures are necessary.
54 Chapter 5
Estimation of the hazard in the case of toxic exposure is based on comparison of

the calculated hazard indices with threshold indices. According to different sources
some hazard index values can be used as the threshold. The following scale is com-
monly used for this purpose (Brebbia 2010):
HQ; HI = 0.2 considered as negligible hazard level,
HQ; HI ≤ 1 considered as acceptable,
HQ; HI  (1; 4) considered as tolerable,
HQ; HI > 4 considered as unacceptable hazard level.
The calculated hazard indices for the scenarios A, B, C and D are 0.00176;
0.00353; 0.0353 and 0.282, respectively. They do not approach unity which is recog-
nized as acceptable limit. The obtained results proved that the risk the service station
workers are facing is negligible and it does not have any negative effect regardless of
the applied scenario. Therefore in both cases of exposure, toxic or carcinogenic, it
should be stated that the environment in the service station is safe.
Any assessment of the health risk has certain margin of uncertainty, resulting from
a limited accuracy of toxic data which are derived from assays on animals and epide-
miological studies. Furthermore, the exposure scenarios include necessary generaliza-
tions emerging when average statistical data are used for calculations. The absorbed
pollutants’ doses depend on the people’s age, gender, individual features of the peo-
ple, their behavior and physiology. All these features affect rates of daily pollutants
absorption by inhalation, water and food ingestion, incidental ingestion of soil or der-
mal assimilation of harmful substances.
Another uncertainty factor is related to analytical errors and the necessity of ana-
lytical results averaging. In order to lower the uncertainties in the calculation, com-
puter aided simulations are used, for instance Monte Carlo analysis involving prob-
abilistic approach to the health risk analysis. It refers to the determination of values
distribution instead of actual figures. In the applied in this work approach it was as-
sumed that the pollutants’ concentrations found in soil remain unchanged within the
exposure period.
Lack of the distinction between specific chemical forms of individual pollutants,
CrIII and CrVI for instance, is a significant generalization relating to the quality of
analyses. Omission of the speciation analysis may be reasonable due to practical and
economical causes.
Full speciation analyses of all pollutants’ chemical forms would be extremely
costly and time consuming. In such a case, when a pollutant might exist in different
chemical forms of different toxicity, it is acceptable to take into account the most
harmful form and assume that it is the only form present in the examined sample. Such
an attitude is commonly called a conservative approach to hazard estimation and it
usually leads to overestimation of the risk. The aim of such proceedings is to ensure
a certain safety margin in the risk assessment.
5.10. Conclusions
In this project estimation of occupational exposure of railway service workers to

anthropogenic pollutants has been carried out. The calculations were made for four
exposure scenarios, for two age groups. Excess lifetime cancer risks and hazard quo-
tients were calculated posed by individual substances, as well as cumulative risk and
hazard index resulting from all the pollutants concerned. It was found that:
 excess lifetime cancer risk in the service station area is negligible and does not
raise concern in respect recognized safety standards and acceptable risk levels.
Cumulative risk ELCRtot for the mostly exposed worker’s group, that is for the
age group 60–64 years and full-shift (8/8) contact with the work stand (ELCR =
1.36 * 10–7) is about 7-fold lower than the acceptable risk (ELCR = 10–6).
 the non-carcinogenic hazard level expressed in hazard quotients HQs and haz-
ard index HI for the all pollutants concerned are very low, as well. They do not
exceed unity which is recognized as the threshold value in toxic hazard consid-
erations. Hazard index for the mostly exposed worker’s group, that is for full-
shift workers (8/8) amounts to 2.82 * 10–1, which means it is equivalent to negli-
gible. Its value is 3 times lower than the acceptable 1.
Despite certain unavoidable assumptions outlining the procedure of the assessment
of the hazards discussed in the above sections of this work it was proven that the fa-
cility is safe. The determined resultants of the exposure, cancer risk and hazard index
fall below any of the acceptable values and thresholds.
6. Environment polluted with chromium
6.1. Background
Chromium can be found in the environment mostly as a result of improper or

careless process management in metallurgical or galvanic plants. Metallurgical plants
are a source of especially burdensome emissions of soil, water and air pollution. They
can negatively affect the environment even after the end of production. Accumulated
waste materials, especially sludge, slag and dusts, have remained as environmental
polluters for years. The former ferrochromium works in Siechnice near Wrocław,
Poland, which used to manufacture alloys for military purposes in the past, is such
a case. The waste dump located near the works contains slag including, among oth-
ers, iron and chromium in different chemical forms. The dump is a reason for con-
cern for the local population and the water treatment company that draws water from
the surrounding area for municipal purposes. Since the time when manufacturing in
the Siechnice metallurgical works was closed down, a variety of plans have been
proposed to solve the environmental problem (Swiat 2012). The most feasible plan
seems to be a recent project assuming the recovery of metallic components, mainly
the ferrochromium alloy, by involvement of multiple operations such as ore extrac-
tion, transport, crushing, screening, magnetic separation, washing, etc. Some of these
processes are accompanied by intensive dust generation, which may create environ-
mental problems.
Chromium is a grey, hard metal most often classified as a heavy metal, commonly
found in compounds in the trivalent state in nature. Trivalent chromium (Cr(III))
is recognized as an essential nutrient and is widely used as a nutritional supplement
for humans and animals. Besides the trivalent Cr(III) form, under certain environ-
mental conditions, chromium can also be found in the metallic zero-valent (Cr(0)) or
the hexavalent (Cr(VI)) forms. The most common ore containing a significant amount
of Cr(III) is chromite (FeOCr2O3). At the beginning of this century, approximately
13.5 million tons of chromite ore were produced and converted into about 5 million
tons of ferrochromium (Papp 2002).
58 Chapter 6
Chromium in different forms can be found in water, soil and air. Natural sources
of chromium are, for instance, rock strata rich in Cr(III)-bearing minerals (chromite
in particular), which dissolve, and subsequently, Cr(III) can be oxidized to Cr(VI)
(Oze et al. 2002).
Anthropogenic chromium sources are effluents from different technological proc-
esses like metallurgy, electroplating, leather tanning, textile dyeing, painting, inking,
and aluminum manufacturing as well as a variety of niche uses (Čáslavský et al.
2010). In the past, green-colored chromated copper arsenate (CCA) used for pressure-
treated lumber was used, contributing to Cr(VI) in the environment. Since January 1,
2004, the US EPA banned the use of CCA-treated lumber for new residential purposes
(Guertin et al. 2004). CCA-treated wood should not be used in raised vegetable beds
or reused in other products such as mulch (EPA 2015).
Chromium concentrations in soils vary from 0 to 1000 mg/kg. The average levels
of chromium in the ambient air in Europe are reported to range between 20–70 ng/m3
(WHO 2000). The concentrations of chromium in ground water also differ substantially
depending on the area concerned. Typically they are placed between 0.3 and 6 μg/L
(Swietlik 1998).
From the environment, people absorb chromium daily from food, beverages, and
ambient air. The daily intake by humans is shown in Table 12 (WHO 2000). In the
case of highly polluted areas, the intake levels can significantly exceed the values
shown in the table.
Table 12. Daily chromium intake doses by humans from different exposure routes (WHO 2000)
Route of exposure Daily intake Absorption

Foodstuff <200 μg <10 μg
Drinking water 0.8–16 μg <1 μg
Ambient air <1000 ng <5 ng
Chromium in the metallic form does not manifest any biological activity while the
trivalent Cr(III) and hexavalent Cr(VI) forms biologically affect the human body. The
two forms differ significantly in the effects produced. Chromium(III) is an important
component of mammals’ diet, whereas the latter is toxic and exhibits mutagenic ef-
fects (WHO 2000; EPA 2015b). Depending on the source of origin, Cr(VI) occurs in
2– –
the form of chromate ion CrO4 , hydrochromate ion HcrO4 or bichromate ion. Hexa-
valent chromium is much less stable than the trivalent form. It easily undergoes re-
duction in the presence of some inorganic ions found in the environment.
The role of Cr(III) in living organisms consists of the control of lipid, peptide and
glucose metabolism. The monitored Cr chemical forms are classified into different
toxicity groups depending on the chemical state and exposure routes. According to the
US EPA, Cr(VI) is classified as group A, (human carcinogen by the inhalation route of
exposure). However, for oral and dermal routes of exposure, it is classified as group D
Environment polluted with chromium 59
(not classifiable as to human carcinogenicity). Cr(III) is also classified as the same

group D (EPA 1998, 2015b).
Cr(VI) is a thousand fold more toxic than Cr(III) because hexavalent chromium is
capable of penetration through the cell membrane while trivalent chromium cannot get
through the biological membranes. Cr(VI) reaching the cell interior may react with
enzymes, DNA and RNA, which disturbs the proper functioning of these molecules. In
further stages of the chemical transformations, destruction of the cells and formation
of cancer cells can occur (Senczuk 2005). Studies of workers in the chromate produc-
tion, plating, and pigment industries consistently show increased rates of lung cancer.
Exposure to Cr(VI) can also cause irritation of the lungs. Prolonged exposure to
Cr(VI) can damage the mucous membranes of the nasal passages and result in ulcers.
In severe cases, exposure may cause perforation of the wall separating the nasal pas-
sages. Exposure to hexavalent chromium can cause skin diseases like dermatitis and
skin ulcers. Allergic reactions to chromium are also reported. The type and intensity of
the adverse health effects strongly depend on the exposure pathway. The worst health
effects resulting in a carcinogenic effect can be expected when Cr(VI) gets to the or-
ganisms with dust in the respiratory system (SAIF 2009).
Because of the above mentioned adverse effects, governments set water, soil and
airborne chromium concentration limits. For example, the Polish chromium occupa-
tional standards in the workplace in dusty air pollutants are as follows: for metallic
chromium, Cr(II) and Cr(III), the maximal allowable concentration is 0.5 μg/L, and
for Cr(VI), it is 0.1 μg/L of air. The maximum short-term exposure limit for Cr(VI)
is 0.3 μg/L (MLSP, 2002). The Ministry of the Health Care established a standard
for chromium in drinking water at 50 μg/L (MHC 2010). The Cr(VI) level is not
standardized. For soil classified to purity class A (intended for residential areas), the
quality standards limit the maximal allowable chromium concentration to 50 mg/kg
(ME 2002).
In the USA, no separate limits of Cr(VI) levels were established in water. The
law regulates only total Cr. The US EPA Drinking Water Maximum Contaminant
Level (MCL) for total Cr is 100 μg/L, while California limits total Cr in drinking
water to 50 μg/L (EPA 2015a).
The presented health risk assessment was carried out at the Wroclaw University of
Technology, Poland, and at the University of Defence, Brno, Czech Republic, based on
chromium concentration analyses in ground water, soil and air. The goal of this study
was to investigate the environmental samples collected from the area affected by the
former ferrochromium plant and the existing waste dump, after the termination of the
manufacturing process in 1990. A further objective was to determine environmental
hazards, particularly the toxic hazards and possible carcinogenic health risks in human
populations exposed to Cr(VI).
It should be noted that the chromium pollution in the environment results not only
from the recent dump emissions but also from the past activity of the production plant.
60 Chapter 6
Reports estimate that during the last years of the plant’s functioning (end of the
1980’s), yearly emission of chromium from point sources was 95 t while the diffuse
emission amounted to 126 t Cr/y (Bilyk and Kowal 1993).
6.2. The site description
The area affected by chromium emissions is located in the vicinity of a site used
for many decades by the metallurgical works that manufactured alloys and other goods
for military purposes. About 3.5 million tons of the ashes, slag and other waste mate-
rials had been accumulated till 1990 when production had been abandoned. The dump
contains remains of the ferrochromium alloys as well as different solids with a relatively
high concentration of heavy metals. Localization of the dump is shown in Fig. 8. It is
situated in the neighborhood of a residential area and is about 300 m southwest from
the aquifers composing water sources for the city of Wrocław.
Fig. 8. Map of the area affected by the chromium waste dump

with the indicated water sampling spots
Nowadays, the dump poses a big problem for the local community. It is a source of
uncontrolled ground, water and air pollution affecting wells, gardens, the growing of
vegetables and fruits and the general living conditions of the town population. The
problem got worse when the local people started to extract waste ferrochromium
pieces from the dump illegally. This kind of activity caused an additional emission to
the environment (Nogaj 2013). Recently a project aimed at the liquidation of the dump
has been initiated. The project concentrates on the recovery of chromium remains and
the utilization of the leftover material as a road construction aggregate. Such activity
may cause elevated dust emission to the environment. Thus, the dump processing
plant requires additional safety measures such as hazard and operability studies
(Najborowski et al. 2017) and occupational risk assessment.
Ground water sampling was carried out from three piezometers installed close to
the residential zone, about 100 meters north and northeast from the dump’s edge, to-
ward the aquiferous area. They were inserted two meters deep into the ground (Fig. 8).
The soil for the analyses was collected from the upper 10 cm ground layer at the same
spots situated next to the piezometers. The ferrochromium waste material was taken
directly from the dump.
Digging, loading and unloading the material generates a dusty fraction spread by the
wind. Chromium, particularly Cr(VI) included in the airborne particulate matter, may
influence machine operators. Therefore, with the purpose of occupational risk deter-
mination, the analyses of ambient air were carried out. They were limited to the
neighborhood of the processing plant. It had been assumed that the airborne dust does
not reach the residential area, at least to a degree that could raise the concerns of the
population. To evaluate an approximate occupational health risk, we had made repeated
measurements, four times in two-week intervals, during working shifts, just in the
closest neighborhood northwards.
6.3. Health risk assessment
The aim of this step of the work was to quantify both the workers’ and residents’
health risk based on the exposure of both population groups to chromium in water, soil
and air. The taken-in doses were determined in compliance with the assumed scenar-
ios and the facts recommended by the EPA (Moya 2011). As the chromium demon-
strates both toxic and carcinogenic effects, quantification was conducted separately for
these effects.
For the purpose of the health effects assessment, methodological principles of the
risk assessment related to polluted areas have been adapted based on the US EPA
guidelines for the “Superfund” project (EPA 1991) with certain modifications. Also,
guidelines for the chromium exposure assessment and possible exposure scenarios pub-
lished by the EPA (1992) have been taken into account. Specific conditions and con-
straints of the area in question required the construction of adequate procedures and
exposure scenarios. The health risk assessment was carried out on the basis of the devel-
oped scenarios, analyses of different chromium forms and the chromium toxicity data.
62 Chapter 6
According to EPA recommendations, a conservative approach to risk assessment

was applied, and thus the greatest potential risk was addressed. For instance, in this
approach, it is assumed that all chromium in the water samples exists in the most
harmful forms, that is in the form of Cr(VI) or Cr(III). This is because these two forms
of chromium undergo conversions from one form to another in water and in the human
body, depending on environmental conditions. Measuring just one form may not cap-
ture these changeable chromium forms.
The following exposure scenarios have been taken into account:
 occupational exposure of workers involved in the waste material processing.
The staff activities comprised mechanical operations at the work site (extracting
the material, loading, transport and unloading, etc.). For this scenario, the non-
carcinogenic hazard level as well as the carcinogenic risk were determined.
 exposure of adult residents comprising lifelong habitation and recreational gar-
den activities in the affected zone. For this exposure scenario, just the intensity
of non-carcinogenic effects, expressed by hazard quotients, was determined be-
cause based on the measurements of the air contaminants, it was assumed that
the residents were not affected by the airborne Cr(VI) form. Gardening and rec-
reation, however, are associated with accidental soil and ground water inges-
tion, which is different for the adults and children.
 Exposure of children in the above mentioned residential zone. There were similar
conditions but different accidental soil and water ingestion doses. The most af-
fected age population was taken into account was the 0–6 year children’s group.
6.3.1. Exposure assessment
The level of chromium in the examined materials differed substantially depending

on the sample type and sampling spot. Sampling of the waste was repeated in 10 dif-
ferent spots of the dump and from different depths, then each sample was averaged.
Contents of Cr in the furnace slag ranged between 0.67E+03 and 47.12E+03 mg/kg of
the dry matter. Except for the slag, other materials like sand, soil, bricks and pieces of
ferrochromium alloy were also found in the waste. The Cr(VI) level ranged between
12.7 and 116.2 mg/kg. For the risk evaluation, the upper value was applied.
Ground water for the analyses was collected from the three piezometers labeled
with letters “w”, “m” and “e.” The sampling was repeated consecutively four times in
the two-week intervals. The results are presented in Table 13.
The average concentration of total chromium in the ground water within the sam-
pling period was 1.13 mg/L. The analyses carried out showed that the level of Cr(VI)
in the water was between 0.00 to 0.04 mg/L, and it underwent substantial changes
with time and location. The average Cr(VI) concentration was 0.02 mg/L.
Table 13. Contents of total and Cr(VI) in ground water collected from
the piezometers (mg/L)
Sampling
Piezometer 1 2 3 4
Cr Cr(VI) Cr Cr(VI) Cr Cr(VI) Cr Cr(VI)
“e” 1.02 0.02 0.08 0.01 0.91 0.04 1.07 0.02
“m” 1.43 0.01 1.22 0.01 1.73 0.03 1.57 0.04
“w” 1.09 0.01 0.99 0.00 1.23 0.02 1.18 0.02
The total chromium level in the soil taken near the piezometers from the depth of
10 cm was between 92 and 186.4 mg/kg with its average value 133.6 mg/kg. The av-
erage Cr(VI) level was relatively low. It ranged from 2.56 to 5.07 to mg/kg, and its
average concentration was 4.13 mg/kg. The Table 14 presents the concentration of
total and hexavalent chromium in the soil.
Table 14. Contents of total and hexavalent chromium in the soil

collected near the piezometers (mg/kg)
Sampling
Piezometer 1 2 3 4
“e” 104.2 2.65 92.6 4.60 99.3 3.98 108.5 4.05
“m” 134.4 3.80 118.6 4.76 128.1 4.43 127.3 2.56
“w” 156.9 4.71 169.0 4.28 186.4 5.07 177.7 4.70
The measurements of airborne dust released from the waste handling area proved
that Cr(VI) was present in the air (Table 15). The average amount of Cr(VI) in the
ambient air was 0.04 mg/m3. It dropped considerably along with increasing the dis-
tance from the waste processing plant area. The average total Cr contents in the air
was 0.36 mg/m3.
Table 15. Contents of total and hexavalent chromium

in the air collected from near the waste processing plant (mg/m3)
Sampling
1 2 3 4
0.44 0.012 0.36 0.022 0.41 0.007 0.21 0.014
64 Chapter 6
Exposure assessment for non-carcinogenic effects

For calculations of Chronic Daily Intakes (CDI) the formulas mentioned below
were applied, determining the chromium doses absorbed by accidental soil and water
ingestion as well as inhalation of airborne dust (Čáslavský et al. 2010):
– Cr by accidental soil (or waste material) ingestion [mg kg–1 day–1]
CDIING, S = cS  IRING, S  FI  EF  ED  BW–1  AT –1  10–6 (19)
– Cr by accidental water ingestion [mg kg–1 day–1]
CDIING, W = cW  IRING, W  FI  EF  ED  BW–1  AT –1  10–6 (20)
– Cr by inhalation of chromium with airborne dust [mg kg–1 day–1]
CDIINH = cA  IRINH  ET  EF  ED  BW–1  AT –1 (21)
where:
cS [mg/kg] is the average concentration of chromium in soil/waste material,
cW [mg/L] is the concentration of chromium in water,
cA [mg/m3] is the concentration of chromium in the air,
IRING, S [mg/day] is the amount of accidentally ingested soil or waste material per
day – 50 mg/day for adults (soil for resident or waste for occupational activity) and
100 mg/day for children (soil) (Moya 2011; EPA 2011b),
IRING, W [mL/day] is the daily amount of accidentally ingested groundwater per day
– 0.075 mL/day for adults and 0.150 mL/day for children applied,
IRINH [m3/h] is the inhaled air rate,
FI  0; 1 is a fraction of the contaminated source (0.3 applied),
EF [day/year] is the exposure frequency,
ED [year] is the exposure duration – 30 years was applied for residents (EPA
1991) and 6 years for the scheduled time of the dump liquidation for the occupational
scenario,
ET [h/day] is the exposure time,
BW [kg] is the average body weight,
AT [day] is the time of exposure during which the concentrations of contaminants
cS, cW and cA are assumed to be constant,
1  10–6 = conversion factor (kg/mg) or (L/mL).
It should be stressed that the above listed parameters have different values de-
pending on the exposure scenario (occupational, adult residents, children). The
chronic daily intakes were determined separately for Cr(III) and Cr(VI) where the
concentration of Cr(III) was intentionally applied as the difference between total
Cr and Cr(VI). That means the conservative assumption of hazard estimation was
used.
Exposure assessment for carcinogenic effects

To determine the carcinogenic risk within the occupational scenario, the inhalation
unit risk IUR was used and the Cr(VI) chronic exposure concentrations (EC) were cal-
culated using the following formula (Braun 2005; Lytle and Woo 2007; EPA 2009):
EC = cA  ET  CF  EF  ED/AT (22)
where:
EC [mg/m3] is the chronic exposure concentration (averaged over a 70-year lifetime),
cA [mg/m3] is Cr(VI) concentration in the air,
ET [h/day] isthe exposure time. It is 8 hours a day in the occupational scenario,
CF is a conversion factor = 1/24 (h  days),
EF is exposure frequency in days/year. In the occupational scenario it is 220 days
a year,
ED [year] is the exposure duration. ED was assumed 6 years as the scheduled time
of the dump liquidation is 6 years.
AT is the averaging time of = 24 hours/day  365 days/year  70 years (lifetime)
= 613 200 hours.
6.3.2. Dose–response relation
The dose–response relation was conducted on the basis of the calculated daily intakes,
chronic exposure concentration and toxicity data (EPA 1992) presented in Table 16.
Table 16. Carcinogenic and toxicity values of chromium (EPA 1992)
Reference Reference Inhalation

Carcinogen NOAEL Dose Concentration Unit Risk
Cr form
classification mg/(kgday) RfD RfC IUR
mg/(kgday) mg/m3 m3/µg
Group D – by the oral
Cr(III) route of exposure (carcinoge- 1.468E+03 1.5E+00 – –
nicity cannot be determined)
Group A – human carcino-
gen by the inhalation route of
exposure.
Cr(VI) 2.5E+00 3.0E–03 1.0E–04 1.2E–02
Group D – by the oral
route of exposure (carcinoge-
nicity cannot be determined)
The determination of the dose–response relation was conducted separately for car-
cinogenic and non-carcinogenic effects.
66 Chapter 6
Dose–non-carcinogenic response relation

In the case of the toxic, non-carcinogenic effects caused by the chromium present
in the environment, the hazard quotient HQ was determined. It was calculated by
comparing the daily doses of a pollutant taken in with the reference doses RfD or
reference concentrations RfC (in the case of the inhalation route). Due to the lack of
a relevant toxicity study addressing the respiratory effects of Cr(III), it was assumed,
based on literature data, that Cr(III) is much less toxic than Cr(VI) and its RfC
is 1000 times higher than for the latter (ATSDR 2008; Dayan and Payne 2001; EPA
1998).
The hazard quotients are expressed by the following formulas (EPA 1992):
HQ = CDI / RfD for the oral intake, (23)
HQ = EC / RfC for inhalation exposure route. (24)
The reference doses RfD and concentrations RfC have to be consistent within the
exposure duration which means that the reference values used should be determined
for appropriate exposure periods. For exposure to multiple non-carcinogenic factors,
the aggregate potential for the non-carcinogenic health effects (the hazard index HI) is
calculated from the following formula:
HI = Σ HQi, (25)
where HQi is a hazard quotient for the i-th factor.
Dose–carcinogenic response relation

The excess lifetime cancer risk ELCR has been determined using chronic exposure
concentrations EC calculated from equation (22). It amounted to 2.4E–04 mg/m3.
Such an approach determines the probability of developing cancer over a person’s
lifetime at a given exposure level. ELCR is expressed by a value representing the number
of extra cancer cases expected in a given number of people, based on exposure to
a carcinogen at a stated dose. The formula is shown below:
ELCR = EC  IUR. (26)
The hazard quotients and excess lifetime cancer risks that were calculated for the
different scenarios are presented in Table 17.
According to Table 17, the hazard indices HI for both children and adults in the
residential scenario have values less than one. Thus, it can be concluded that the pol-
lutants should not cause harmful toxic effects in the population. On the other hand, the
HI value for the occupational scenario exceeds the safe level almost 30 times. The
main harmful factor contributing to such a high hazard is exposure to the Cr(VI) pres-
ent in the dust. Such a value is absolutely not acceptable; therefore, some protective
measures are necessary for hazard reduction.
Table 17. Hazard quotient HQi, hazard index HI

and excess lifetime cancer risk (ELCR
Residents
Exposure type Workers
adults children
HQ – Residential activity
ground water ingestion Cr(III) – 6.8E–10 3.6E–09
soil ingestion Cr(III) – 5.3E–05 2.8E–04
ground water ingestion Cr(VI) – 6.2E–09 3.3E–08
soil ingestion Cr(VI) – 8.5E–04 4.5E–03
HI – Residential activity – 0.142 0.757
HQ – Occupational activity
inhalation Cr(III) 7.0E–01 – –
inhalation Cr(VI) 2.8E+01 – –
waste ingestion Cr(III) 6.0E–03 – –
waste ingestion Cr(VI) 1.5E–02 – –
HI – Occupational activity 2.9E+01 – –
ELCR – Occupational activity inhalation 2.9E–03 – –
Regarding the carcinogenic hazard, the calculated risk in the occupational scenario
amounts to 2.9E–03. According to the accepted standards, such a risk level is also
unacceptable. A risk level approaching 10–3 absolutely requires protective measures.
In general, the US EPA considers excess cancer risks that are below 1 chance in
1 000 000 (110–6 or 1E–06) to be small enough for regarding them as negligible and
risks above 1E–04 to be sufficiently large that some sort of remediation is desirable.
In order to lower the occupational non-carcinogenic hazards as well as the car-
cinogenic risk, it is necessary to apply some effective measures to reduce dust emis-
sion and protect the workers. We would recommend developing, if possible, wet op-
erations and wet processing of the waste material. Sprinkling the waste material with
water could be advisable. Also dust extraction attachments, dust filters and particu-
larly individual protection accessories like dust masks, dust protective cabins, etc.
should be prescribed.
As far as the residents are concerned, the waste dump does not arouses any reser-
vations related to the health standards. The calculated HQ values do not exceed unity,
both for adults and children.
6.3.3. Uncertainty analysis and discussion
It should be emphasized that the obtained results have to be interpreted cau-

tiously, taking into account numerous conscious uncertainties and simplifications
made during the risk considerations. They could not be avoided because of certain
inevitable assumptions. Nevertheless, the obtained results made it possible to evalu-
68 Chapter 6
ate the hazard and health risk levels expected at the sites affected by the chromium
waste dump.
The ambiguities result from the imperfection of the chemical analyses, the simpli-
fying assumptions and the incompleteness of some toxicological data on chromium
toxicity. The procedure presented here is based on the conservative approach to risk
assessment, which tends rather to overestimate than underestimate the risk. The main
factors contributing to assessment uncertainty are:
 The lack of routine and systematic data from monitoring of the environmental
samples collected at the area concerned. It is not known whether the concentra-
tions of chromium in groundwater, soil and especially in the air will remain at
a constant level over the longer period of exposure time.
 The concentration of dust in the air strongly depends on weather conditions, air
humidity, wind direction and speed, etc. This implies severe fluctuations in the
measured values affecting the risk calculations.
 Because of the lack of data on the absorption coefficients of chromium in the hu-
man body, the coefficient was assumed to be equal to 1 for all the chromium forms.
 There was no distinction made between different chromium forms for the hazard
quotients calculations. For that purpose, for the Cr(III) hazard calculations, the total
chromium contents reduced by Cr(VI) contents was applied, which could involve
an overestimation of the hazard posed by trivalent chromium. In fact, such an ap-
proach did not have a significant contribution to the Cr(III) hazard quotients.
6.4. Conclusions
The investigations of the chromium emissions from the waste dump showed quite
high concentrations of its trivalent and hexavalent forms in the environment. The level
of non-carcinogenic hazards determined for the residents’ scenario does not arouse
any concern both for adults and children. The situation is completely different in the
case of the occupational exposure scenario related to waste dump processing. The
calculated carcinogenic risk is extremely high, which implies the necessity of careful
revision of all unit operations included in the waste processing line in respect to haz-
ard reduction. The major hazard is connected to dust emissions to the environment.
The same remarks concern the non-carcinogenic hazards and calculated hazard quo-
tients, which strongly exceed the acceptable standards.
Under the current toxicity standards, the investigated occupational activity requires
protective measures in order to reduce the workers’ exposure to dust emissions. There
are relatively simple methods of exposure reduction available, which certainly should
be implemented by the contractor during the industrial processing of the waste.
7. Nitrogen compounds in the surface waters
7.1. Background
Water is an important geological and climatic factor which enters into the compo-
sition of plant and animal tissues. It is also a habitat of variety of living organisms. For
people, water composes a medium widely used in different types of economic activity,
however water is mainly used for consumption. For this purpose water is drawn from
variety of sources. In many areas surface water is used after treatment processes that
ensure the removal of pollutants.
From among water contaminants, particularly burdensome are the inorganic nitrogen
compounds. They are easily soluble which makes their removal from water very difficult.
−
Inorganic nitrogen compounds in the surface waters, actually nitrate(V)-ions (NO3 ) and
−
nitrite(III)-ions (NO2 ), which are commonly called nitrate and nitrite ions, are mostly
of anthropogenic origin. In majority, they originate from agriculture and industry.
Untapped by plants, the nitrogen compounds migrate with the soil solutions to sur-
face and ground waters finding their way to reservoirs of raw water intended for mu-
nicipal use. Nitrate emission is very destructive to environment. Firstly it brings about
negative effects, eutrophication in the first place, consisting in “bloom” or great increase
of phytoplankton in a water body. Adverse environmental phenomena include hypoxia,
the depletion of oxygen in the water, which causes decrease in specific fish and other
animal populations. In regards to the health effects, nitrogen compounds can cause seri-
ous diseases which intensity depends on the absorbed dose and type of the compound.
To reduce nitrogen run off from agricultural area the Nitrates Directive has been
accepted by the European Commission, controlling the nitrogen fertilizers application
(EU 1991). According to this document, negative effect of nitrogen compounds on
environment can be reduced by continuous monitoring of surface waters’ quality, fol-
lowing the good agricultural practice rules and the implementation of law regulations
related to waste management and handling of chemicals Municipal sewage and indus-
trial waste waters are the second nitrogen source in the waters. In the presented study,
problem of water pollution with nitrates in the Mała Panew river flowing in southwest
Poland was discussed to determine the resulting health threats. The aim of the work
70 Chapter 7
was to investigate the pollutants level in the river and compare the obtained results
with obligatory drinking water standards. The results were then applied for quantita-
tive determination of probable health hazard, which could occur if the river water was
to be considered as a source of drinking water. Such fears were manifested during
talks with the local community.
The origin of nitrates in the river Mała Panew is obvious because it flows through fer-
tilized arable area which composes a non-point source of nitrogen compounds in the wa-
ter. The fertilizers used on surrounding farmland are not completely absorbed by crops and
migrate to smaller and bigger watercourses running into the river. Also cases of uncon-
trolled animal breeding effluents are known, which drain into the watercourses. The sec-
ond known source of nitrates, a point source, is the emission from a chemical factory in
Krupski Młyn, manufacturing nitro-organic products, explosives among others. In the
manufacturing process nitric acid is used and a significant amount of it passes to waste
waters. After preliminary treatment with hydrated lime, the waste waters are dumped into
the river. The treatment process is characterized by insufficient effectiveness to catch all
–
contaminants. Analyses showed that average concentration of NO3 in the waste waters
–
after treatment, dumped directly into the river, is about 7900 mg/dm3. When NO2 is con-
sidered, only traces of this nitrogen form were found in the waste water. Yearly 9 thousand
cubic meters of such waste waters is produced in the company. As a result increased level
of nitrate ions are observed in the river (Pawełczyk 2008).
7.2. Sampling spot
Sample collection spot was located next to the bridge in the village Żędowice in south-
west Poland, on the river Mała Panew flowing across Silesia and Opole regions (Fig. 9). The
water samples were collected every second week during the period of 7 months.
Fig. 9. Location of the chemical factory and sampling spot along the river
Nitrogen compounds in the surface waters 71
7.3. Results of water analyses
Results of nitrate(V) and nitrate(III) analyses in the river, during the period of
about 7 months show Figs. 10 and 11.
5
4
NO3 [mg/dm ]
3
1
0 5 10 15 20 25 30
sampling week
Fig. 10. Concentration of nitrate(V) in the river [mg/dm3]
0.038
0.036
0.034
0.032
NO2 [mg/dm ]
3
0.030
0.028
0.026
0.024
0.022
0.020
0 5 10 15 20 25 30
sampling week
Fig. 11. Concentration of nitrate(III) in the river [mg/dm3]
The concentrations of both nitrogen anionic forms vary depending on the time
the sample was collected. The highest nitrate content occurs between 10-th and 20-th
72 Chapter 7
week of the sampling period, i.e., between end of May and middle September. Low-
est concentration was observed during the initial weeks of water monitoring period,
that is in April. It is obvious that the nitrogen concentration trends are associated
with fertilization period and weather conditions. These two factors overlap, contrib-
uting to the increase of nitrate level in the river water. During the spring time more
fertilizers are used by farmers and this source is predominant. On the other hand,
more intensive rainfalls occur during this period, flushing off the easily soluble ni-
trogen compounds from the fertilizers. This should result in higher concentration of
nitrates in the watercourses. However the rainfalls and higher water flow in the
river, additionally triggered by snow melting, compensate to some degree, the nitro-
gen concentration. The highest nitrogen level occurs during the summer time, when
the rainfalls are limited.
–
The average concentration of the NO3 over the whole investigation period was
–
3.54 mg/dm3. In the case of NO2 the highest concentration was during the first 6 weeks,
the lowest occurred twice: between 10-th and 12-th and between 22-th and 26-th week.
–
Average contents of NO2 in the river water amounted to 0.286 mg/dm3. In respect of
nitrate(V) and nitrate(III) concentration, water from the river could be classified to the
first and second purity class of inland waters, respectively. The highest permissible
–
limits of nitrates for the first class water are: 5 mg/dm3 of NO3 and 0.03 mg/dm3
–
of NO2 (ME 2004).
For the purpose of the health effects estimation, methodological principles of the
health risk assessment related to polluted areas have been applied, based on US EPA
guidelines for “Superfund” project (EPA, 1980). The methodology has been published
in the Risk Assessment Guidance for Superfund (EPA 1989).
Although nitrates are not reported to have carcinogenic effect on humans, they are
precursor compounds in the formation of N-Nitroso compounds, many of which can
be human carcinogens (Cohen 1996). Anyway, carcinogenic effects of nitrates in wa-
ter are not proven sufficiently. With respect to the chronic effects, there are no clear
evidences for adverse health effects related to ingestion of nitrates. The epidemiologic
studies of cancer do not support an association between ingestion of dietary nitrate and
an increased risk of cancer (Grinsven et al. 2006). Additionally no health values are
available so far, that could be applied for quantification of carcinogenic risk.
However nitrates can bring about serious toxic adverse effects, particularly in in-
fants under the age of six months. High concentration of nitrates in water can cause
methemoglobinemia also called “blue baby syndrome”. This illness occurs especially
in infants under six months of age as their stomachs contain much weaker acid than in
older children and adults. In such favorable conditions, more bacteria develop which
– –
can readily convert nitrate(V) (NO3 ) to nitrate(III) (NO2 ).
The latter is then absorbed by the blood, and converts hemoglobin (the oxygen-
carrying component of blood) to methemoglobin. Thus, oxygen cannot be carried effi-
ciently in the baby’s body. As a result vital tissues such as the brain, is not supplied
with oxygen in sufficient quantities. Unlike in infants, methemoglobin changes back
to hemoglobin in adults. Methemoglobinemia can result in brain damage and death.
Apart from infants, the most sensitive to methemoglobinemia are pregnant women,
people with a deficiency of the enzyme converting methemoglobin back to normal
hemoglobin, and adults with low stomach acidity (Senczuk 2005).
No such effects are observed at low nitrates’ concentrations. Therefore maximal
levels of the nitrates have been set in drinking water. The national drinking water
regulations in the USA set the maximum contaminant Level MCL for nitrates(V) and
nitrates(III) for 10 and 1 mg/dm3, respectively (EPA 2011a, EPA 2017b). The current
standards for nitrate level in drinking water set by the Polish Ministry of Health Care
are 50 mg/dm3 of nitrate(V) and 0.5 mg/dm3 of nitrate(III) (MHC, 2007). At the same
– – –
time the following condition must be met: [NO3 ]/50 + [NO2 ]/3 ≤ 1, where [NO3 ] and
–
[NO2 ] are concentrations of nitrate(V) and nitrate(III), respectively. Additionally the
–
NO2 concentration in the water introduced into the water supply system and other
water distribution facilities should not exceed 0.10 mg/dm3.
The dose-response relation has been discussed in respect of oral exposure because
ingestion with water is the main pathway for nitrates into individual’s body. Dermal
exposure affects the health to a lesser degree. As the contaminants concerned are sus-
pected to produce toxic (non-carcinogenic) adverse health effects, the dose-health
response relation was determined solely for such effects, on the basis of the available
toxicity data. Since infants are the subpopulation most susceptible to nitrate induced
methemoglobinemia, the assessment was limited to that age group and additionally
extended to other children’s age groups up to 3 year-old. The older children and adults
were not taken into consideration because it is likely, that they do not respond with
increased methemoglobin to nitrate in drinking water.
For evaluating the non-carcinogenic effects a “reference dose” (RfD) was applied.
RfD has been derived from the so called “no-observed-adverse-effect-level” (NOAEL),
that is from highest concentration (or dose) of a toxic substance, that produces no
health effects. When the threshold concentration is exceeded the adverse effects start
to manifest. Table 18 shows toxic characteristics of nitrates, set on the basis of met-
hemoglobinemia observed after ingestion of polluted water.
74 Chapter 7
Table 18. Toxicity of nitrates and nitrites related to methemoglobinemia

as a critical health effect (EPA 2017a)
Pollutant RfD NOAEL
Nitrate(V) 1.6 [mg/(kgday)] 1.6 [mg/(kgday)]
Nitrate(III)* 0.1 [mg/(kgday)] 1.0 [mg/(kgday)]
* Infant chronic exposure to drinking water.
The above data were used to determine the expected health effects. For that pur-
pose hazard quotient HQ was determined, for which the formula (27) is applicable. It
should be emphasized, that the HQ has nothing to do with risk, which is normally
expressed as probability and applies to the carcinogenic instances (Biesiada 2000).
HQ is calculated by comparing the average daily doses ADD of pollutants taken in
(see the explanation below), with the reference doses RfD (EPA 1992):
HQ = ADD/RfD (27)
The ADD – average daily dose or exposure level (intake) expressed in [mgkg–1d–1]
is calculated for each pollutant separately, depending on the exposure durations.
The aggregate potential for the non-carcinogenic health effects resulting from
multiple hazardous substances – the hazard index HI, was calculated from the for-
mula (28):
HI = Σ HQi (28)
Quantification of exposure to water pollutants has been made in similar way to that
for non-carcinogenic effects, using formula (29). Since small children are most sensi-
tive to nitrates in water, children’s sub-populations up-to-3-years-old, including in-
fants, were taken into account in the health effects estimation (6 age groups in total).
Since there are not clear evidences for carcinogenic effects of nitrates in water, acute
effects, not chronic, were considered and for shorter-term exposure duration (less than
2 weeks), namely for one week. For the all age groups considered, the averaging times
were the same as exposure durations. The child-specific exposure factors, that is age,
body weights, daily community water intake doses and daily bathing times are shown
in Table 19.
The use of total water ingestion rates, including bottled water, might overestimate
the potential exposure to nitrates. Thus, EPA estimates of tap water ingestion for par-
ticular age groups were used (EPA 2008).
Table 19. Child specific exposure factors applied for exposure quantification.
Bottled water, beverages and water included in purchased foods is not taken into account (EPA 2008)
Body Community water Mean skin Mean bathing

Age group weight intake daily doses surface area (event) time
[kg] [dm3/day] [m2] [min/day]
Birth to 1 < month 4.8 0.184 0.29 19
1 to < 3 months 5.9 0.227 0.33 19
3 to < 6 months 7.4 0.362 0.38 19
6 to < 12 months 9.2 0.360 0.45 19
1 to < 2 years 11.4 0.271 0.53 23
2 to < 3 years 13.8 0.317 0.61 23
Two types of exposure were taken into consideration: oral and dermal. Quantifica-
tion of oral exposure related to community water ingestion has been made using for-
mula (29) which applies to each pollutant (NO3– and NO2–) and to each age group sepa-
rately (EPA, 1989):
ADDoral = c  FI  (IR  EF  ED)/(BW  AT) [mg  (kg  d)–1] (29)
where the particular formula parameters are adapted to calculation of the acute toxic
substances intakes. In this way:
ADDoral is the Average Daily Dose for oral exposure,
c represents the average concentration of NO3– or NO2– in water [mg/dm3],
FI is an absolute number in the range of 0–1, specifying contribution of the par-
ticular pollution sources to the pollutant intake by the children. In the following cal-
culation the FI factor is not applicable as only community water intakes, not total wa-
ter, were taken into account. Bottled and beverage water was excluded from the
consideration. The community water intakes by the specific age groups are given in
Table 19, according to (EPA 2008). Thus, FI = 1.
IR represents the intake rate of community water. For the particular age groups the
daily water intake rates, according to (EPA 2008), are given in Table 19.
EF – the exposure frequency = 7 days/week for all children’s groups.
ED – the exposure duration. For all children’s age groups it is the same as the
acute effect, not longer term effect is considered. Thus, ED = 1 week.
BW – the average body weight. For particular age groups the body weights are
given in Table 18.
AT – the averaging time. For acute effects it is the same as the exposure duration.
AT = 7 days for all age groups.
Second exposure pathway taken into account is absorption through the skin during
bathing events. Nitrates permeate through the skin reaching circulatory system. To
determine this exposure portion, dermal permeability coefficients of nitrates and ni-
trites have to be used in calculations. As their values are not known, permeability co-
efficient for water was used. Such an approach assumes, that the pollutants freely
76 Chapter 7
permeate with water through the skin, not being stopped by the skin tissue. The water
permeability coefficient Kp is 1.5E–04, according to (EPA 2004). Dermal absorbed
dose per bathing event DAevent for inorganic compounds dissolved in water can be
calculated from the formula (30):
DAevent = Kp  c  tevent [mg  (m2  event)–1] (30)
where:
– –
Kp represents dermal permeability coefficient of NO3 or NO2 in water [m/h],
tevent is the daily event duration [min/event] – see the Table 19.
Table 20. Individual average daily doses ADD of nitrates and nitrites,
taken in by all age subpopulations absorbed by water ingestion
and dermal contact [mg  kg–1  d–1]
Sub-population ADDNO3 ADDNO2

Birth to < 1 month 0.136 0.011
1 to < 3 months 0.136 0.011
3 to < 6 months 0.173 0.014
6 to < 12 months 0.139 0.011
1 to < 2 years 0.084 0.007
2 to < 3 years 0.081 0.007
Knowing body weight, skin surface area and mean time of bathing event for par-
ticular children’s age groups, the dermal absorbed dose per bathing event DAevent can
be easily converted to dermal Average Daily Dose (ADDdermal). The total Average
Daily Dose (ADD), as a sum of oral and dermal exposures is calculated from:
ADD = ADDoral + ADDdermal [mg  (kg  d)–1] (31)
The calculated average shorter term Average Daily Doses for oral and dermal ex-
posures are shown in the Table 20.
7.7. Hazard characterization
Quantification of impact of the considered water pollutants on the examined sub-

population’s health has been carried out on the basis of the absorbed doses, using for-
mula (27). Comparison of the average daily doses ADD with reference doses RfD en-
abled to determine the health threat level in case of using the water for children’s con-
sumption and bathing. Table 21 shows the hazard quotients HQ due to the
contamination of water with both types of nitrates, calculated for the particular sub-
populations. Also a hazard indexes for the sum of HQs determined for the both pollut-
ants are given in the table.
Table 21. Hazard quotients HQ and a hazard indexes HI

for the children sub-populations
Sub-population HQ-NO3 HQ-NO2 HI

Birth to < 1 month 0.085 0.110 0.195
1 to < 3 months 0.085 0.110 0.195
3 to < 6 months 0.108 0.140 0.248
6 to < 12 months 0.087 0.112 0.198
1 to < 2 years 0.053 0.068 0.121
2 to < 3 years 0.051 0.066 0.117
As one can notice, both the HQ and the HI connected with the water pollutants are
below unity for all sub-populations. These satisfactory results are due to the custom of
using partially bottled water replacing tap water for consumption. The calculated haz-
ard indexes would be much higher in case of using community water only. They might
approach the critical HI value, when other additional nitrate sources would be consid-
ered. As expected, the older children’s population is, the lower chance for adverse
effect manifested by methemoglobinemia. But surprisingly, for the 3-to<6 and 6-to<12
months children’s groups, the hazard indexes are the highest. This is probably due to
the higher consumption of community water by these sub-populations in relation to
their mean body weights.
It should be concluded that under the applied assumptions, the nitrates and nitrites
do not cause serious harmful health effects in the considered sub-populations. It would
be advised however, to control other nitrates’ sources possible, for instance vegeta-
bles, fruit, meat, dairy products etc. Younger infants, these under 3 months old are not
expected to consume that kind of food, except of milk. In case of children over 3
months old any additional pollutants’ pathways could bring about increased HI values
and chances for nitrate-caused adverse effects. Generally nitrites contribute considera-
bly worse to the health hazard than nitrates, even though their concentration in water
is several times lower than the latter.
The ADD, HQ and HI calculations carried out have practical meaning because they
inform if the river water can be safe for consumption. The aim of the study was just to
prove if the water could be used as a raw water source for municipal purposes, in re-
spect of nitrate contents. The main factors contributing to assessment uncertainty are:
78 Chapter 7
 no systematic data available from monitoring of water from the river over the
whole year;
 the concentrations of the pollutants in the water do not remain constant and they
vary depending on the water level in the river, season etc. For the purpose of
determination of trends, longer sampling period, at least one year, would be
recommended;
 the relation between both nitrogen forms changes in time cannot be determined,
which complicates the assessment and affects the results;
 nitrate toxicity values are not available in literature for all sub-populations con-
sidered. It was assumed that within the age groups concerned, the values from
infants could be adopted, which makes the evaluations more conservative;
 there are no data available on nitrate permeability coefficient, necessary for
dermal exposure calculation. For this purpose, water permeability coefficient
was applied, which means that nitrates can freely permeate through the skin
along with water and are not stopped by the skin tissue.
7.9. Conclusions
The evaluation of health effects related to nitrate(V) and nitrate(III) in water has
shown that the levels of these compounds meet water purity standards. The nitrogen
compounds in the water originate from nonpoint sources, chiefly from agricultural
areas as well as from point source, that is from waste waters dumped by a chemical
factory located about 10 kilometers upstream the sampling spot.
As regards the risk of toxic effects, the calculated hazard quotients HQ and hazard
indexes HI do not give a cause for concern, however the HI could approach critical
unity value in case of an increase in community water consumption instead of bottled
water. For that reason it is not recommended to consider the river as a prospective
municipal water source, unless its purity standard is improved. Other possible nitrate
sources like vegetables, fruit, meat, dairy products etc, can contribute to an increase of
toxicity indexes. For that reason it would be recommended to control community wa-
ter consumption.
Under the current toxicity standards, when oral and dermal pathways are taken in
consideration, the investigated river water is safe for all children’s sub-populations, as
regards non-carcinogenic health effects discussed.
Nitrites present in the river water contribute much more to the methemoglobinemia
health threat, than nitrates, even though their concentration in the river is several times
lower than the latter.
8. Persistent organic pollutants
in drinking water supply system
8.1. Background
The following section refers to persistent organic pollutants represented in this

case study by polychlorinated biphenyls and organochlorine organic pesticides.
They were used on a massive scale in not so distant past still pose major health haz-
ard to people and animals. Polychlorinated biphenyls are a mixture of congeners
differing in their composition. Theoretically, 209 congeners produced by the chlori-
nation of biphenyl are possible (Snell et al. 2007). These compounds have different
trade names, such as: Aroclor in the USA, Phenochlor in France, Clophen in Ger-
many, Kanechlor in Japan, Fenchlor in Italy, Sovol in Russia and Delor in the former
Czechoslovakia. Industrial polychlorinated biphenyl preparations called Chlorofen
and Tarnol were produced in Poland. Polychlorinated biphenyls are characterized by
low reactivity, are fire-retardant and poorly biodegradable (Falandysz et al. 2007).
The recommended chemical nomenclature of polychlorinated biphenyl congeners
used further in this work is referenced to (Mills et al. 2007). It was mainly owing to
these properties that PCBs were commonly and widely used in industry. Polychlori-
nated biphenyls were chiefly used as additives to electrical oils, compressor oils,
hydraulic oils, paint improvers, impregnating agents, anti-dust agents, plasticizers
for plastics, rubber softeners and heat-carrying agents. Because of the proven harm-
ful effect of polychlorinated biphenyls on living organisms their production and use
were discontinued. Polychlorinated biphenyls, similarly as organochlorine pesti-
cides, were labeled as toxic organic compounds TOCs. Similar restrictions were
imposed on the use of chlorinated pesticides.
Chlorinated pesticides contributed to a reduction in diseases, higher crops and in-
creased animal production. Hexachlorocyclohexane and p,p-Dichlorodiphenyltrichloro-
ethane (DDT), as well as the persistent organochlorine compounds from its decompo-
sition, are still present in the environment, despite the ban on their use introduced in
80 Chapter 8
most countries in the 1970s. Over time p,p-Dichlorodiphenyltrichloroethane decom-

poses into p,p-Dichlorodiphenyldichloroethylene (DDE) and p,p-Dichlorodiphenyl
dichloroethane (DDD), which have similar physical, chemical and toxicological prop-
erties. As they pass through the food chain the substances accumulate in human and
animal organisms, mainly in their fatty tissue and internal organs. Thirty three years
after its banning in the US, p,p-Dichlorodiphenyltrichloroethane is still detectable in
about 10% of the population while p,p-Dichlorodiphenyldichloroethylene (DDE)
occurs in almost everyone (Eskenazi 2006).
The use of polychlorinated biphenyls and pesticides have led to the accumulation
of these compounds in the environment and their migration, resulting in the contami-
nation of waters, including drinking water intakes. Polychlorinated biphenyls get into
the environment through evaporation and leakages and during incineration, industrial
sewage discharge and waste disposal. It is estimated that about 80% of the annual
production of Polychlorinated biphenyls would get into the environment in this way
(Nisbet and Sarofim 1972). Atmospheric conditions play a major role in the transport
of organochlorine pesticides. The concentration of the pesticides in water increases
when the thaw begins, whereby they are then detected in mountain waters and even in
the polar regions. When they get into the atmosphere polychlorinated biphenyl vapors
are absorbed on the suspended dust particles. The average concentration of poly-
chlorinated biphenyls in air in different areas of Sweden amounted to 1–50 ng/m3
(PZWL 1985). In environmental hazard conditions less than 5% of the dose absorbed
by the body comes from absorption through the respiratory tract and the skin. The
other 95% of the dose is absorbed through the alimentary canal (Koopman-Esseboom
et al. 1994).
Analyses of the water drawn for consumption purposes from the intakes in one of
the districts near the city of Wrocław showed a surprisingly high level of its contami-
nation with persistent organic pollutants POPs such as polychlorinated biphenyls and
organochlorine pesticides (Pawełczyk et al. 2008a) in comparison with standards for
drinking water (MHC 2000, EPA 2011a). The cause of the presence of these pollut-
ants in the investigated water intakes has not been explained yet. Probably the poly-
chlorinated biphenyls infiltrate into water mainly in places where industrial and mu-
nicipal sewage is discharged into rivers.
Solubility of polychlorinated biphenyls is low and decreases with increasing chlo-
rine content. Sewage treatment does not remove dissolved fraction of polychlorinated
biphenyls from water, therefore they pass from the sewages to various water reser-
voirs. Due to hydrophobic properties polychlorinated biphenyls tend to absorb on sus-
pended solid organic and inorganic particles and only that part of PCBs can be easily
separated from water.
Dissolved polychlorinated biphenyls pass also through commonly used raw water
treatment systems (Starek 2001). The widespread sand beds are not capable of ad-
Persistent organic pollutants in drinking water supply system 81
sorbing the dissolved organic compounds. For that purpose activated carbon systems
or other techniques would be suitable, which increase costs of the water treatment
processes.
The main objective of the work was to determine the contribution of selected POP
contaminants present in the water intakes, to excess adverse health effects, among the
local population consuming the water. Actually the so called Excess Lifetime Cancer
Risk ELCR for cancer effects and the so called hazard quotient for non-cancer effects
originating from polychlorinated biphenyls and pesticides in water was discussed. The
research should determine if any measures have to be taken in order to abate the expo-
sure of the population to these particular contaminants’ groups.
The health risk assessment presented in the paper was conducted according to the
procedure recommended by the US EPA in Risk Assessment Guidance for Superfund
(EPA 1989). It includes hazard identification, dose–response assessment, exposure
assessment, risk characterization and uncertainty analysis.
8.2. Results of water analyses
Raw water taken from three deep wells located in the vicinity of a county town near
Wrocław was analyzed. Also water samples taken from a small river flowing through
the protected area of the district’s water intakes were examined. The chemical analyses
showed that congeners: 2,2,5-Trichlorobiphenyl (PCB18), 2,3,3-Trichlorobi-
phenyl (PCB20), 2,4,4-Trichlorobiphenyl (PCB28), 2,2,3,5-Tetrachlorobiphenyl
(PCB44), 2,2,5,5-Tetrachlorobiphenyl (PCB52), 2,2,4,5,5-Pentachlorobiphenyl
(PCB101), 2,3,4,4,5-Pentachlorobiphenyl (PCB118), 2,3,3,4,4-Pentachlorobiphenyl
(PCB105), 2,2,4,4,5,5-Hexachlorobiphenyl (PCB153), 2,2,3,4,4,5-Hexachloro-
biphenyl (PCB138), 2,2,3,3,4,4,5-Heptachlorobiphenyl (PCB170), 2,2,3,4,4,5,5-
Heptachlorobiphenyl (PCB180) and 2,2,3,3,4,4,5,5-Octachlorobiphenyl (PCB194)
were present in the water intakes. Also organochlorine pesticides were found in the
water.
Except of p,p-Dichlorodiphenyldichloroethylene (DDE), the lower quantification
limits both for polychlorinated biphenyls and the pesticides were 1 ng/dm3. For p,p-Di-
chlorodiphenyldichloroethylene the limit was 5 ng/dm3.
Tables 22 and 23 show the averaged results of analyses for the persistent organic
pollutants monitored in the three water intakes and in the river flowing through the
water-bearing areas in the period of 5 months. The samples were collected every
week, that means the each average value was obtained from about 20 determinations.
The average contents of PCBs and organochlorine pesticides from the three wells were
451.96 and 73.53 ng/dm3, respectively.
82 Chapter 8
Table 22. Qualitative and quantitative PCBs composition of water samples

from three wells and river [ng/dm3]
CAS Well Well Well Average
Analyte River
Number I II III I–III
PCB18 2,2',5-
37680-65-2 2.44 285.87 131.33 139.88 44.31
Trichlorobiphenyl
PCB20 2,3,3'-
38444-84-7 0.78 15.29 0 5.36 672.74
Trichlorobiphenyl
PCB28 2,4,4'-
7012-37-5 128.23 6.27 241.62 125.37 –
Trichlorobiphenyl
PCB44 2,2',3,5'-
41464-39-5 167.65 8.56 118.66 98.29 485.27
Tetrachlorobiphenyl
PCB52 2,2',5,5'-
35693-99-3 0 0.14 179.46 59.87 –
Tetrachlorobiphenyl
PCB101 2,2',4,5,5'-
37680-73-2 0 3.44 8.53 3.99 2.18
Pentachlorobiphenyl
PCB118 2,3',4,4',5-
31508-00-6 6.12 1.17 0 2.43 –
Pentachlorobiphenyl
PCB105 2,3,3',4,4'-
32598-14-4 0.03 7.85 3.21 3.70 1.46
Pentachlorobiphenyl
PCB153 (2,2',4,4',5,5'-
35065-27-1 0 1.67 7.22 2.96 6.74
Hexachlorobiphenyl)
PCB138 2,2',3,4,4',5'-
35065-28-2 7.62 4.13 4.02 5.26 8.54
Hexachlorobiphenyl
PCB170 2,2',3,3',4,4',5-
35065-30-6 5.43 8.07 0.69 4.73 2.13
Heptachlorobiphenyl
PCB180 2,2',3,4,4',5,5'-
35065-29-3 0 0.11 0 0.04 –
Heptachlorobiphenyl
PCB194 2,2',3,3',4,4',5,5'-
35694-08-7 0 0 0.24 0.08 7.34
Octachlorobiphenyl
Total 318.30 342.57 694.98 451.96 1230.71
Table 23. Organochlorine pesticides contents in water samples

from three wells and river [ng/dm3]
CAS Well Well Well Average

Analyte River
Number I II III I-III
1,2,3,4,5,6-Hexachlorocyclohexane
58-89-9 3.26 98.17 65.74 55.72 153.86
(gamma-HCH)
p,p'-Dichlorodiphenyldichloroethylene
72-55-9 (p, p-DDE) 6.21 4.84 0 3.68 0.02
(DDE)
p,p'-Dichlorodiphenyl dichloroethane
72-54-8 (p, p-DDD) 10.48 2.85 4.65 5.99 7.48
(DDD)
p,p'-Dichlorodiphenyltrichloroethane
50-29-3 14.39 6.65 3.31 8.12 6.63
(DDT)
Total 34.34 112.51 73.70 73.53 167.99
The concentrations of the organochlorine compounds vary between the particular

intakes. Besides the water from the river, the highest pollutants’ contents occurs in in-
take III. From among polychlorinated biphenyls, the investigated intakes contain most
2,2,5-Trichlorobiphenyl and 2,2,3,5-Tetrachlorobiphenyl and from among pesticides,
they contain most 1,2,3,4,5,6-Hexachlorocyclohexane (gamma-Hexachlorocyclo-
hexane, gamma-HCH). The average pollutants’ contents calculated for all the intakes
for the whole monitoring period amounts to 451.95 and 73.53 ng/dm3 for respectively
polychlorinated biphenyls and pesticides (Pawełczyk 2010). Some of the given values
are very insignificant and below the quantification limit. However they were given to
realize that certain compounds were detected in water in very low concentrations but
they should not affect the risk level in any meaningful way.
No regularity and systematic trends were observed that could be a ground for rea-
sonable conclusions related to the concentrations’ anticipation.
Reports on possible adverse health effects caused by polychlorinated biphenyls

and organochlorine pesticides and the products of their decomposition arouse much
interest among specialists involved in the assessment of the health risk connected with
the presence of these pollutants in the environment. The epidemiological assays
showed that the persistent organic pollutants negatively affect living organisms and
disturb their hormonal balance and normal biological functioning. As a result, repro-
ductive organs failures, immunological system handicaps, tumor and cancer formation
and defects of major internal organs can occur. In many cases, the consequences of the
exposure to the pollutants appear after a long time, sometimes in maturity or in the
subsequent generations.
The monitored substances are classified into group B2 (possibly carcinogenic to
humans), except for gamma-Hexachlorocyclohexane (gamma-HCH) which has not
been classified by EPA. None of the pollutants detected in the water was classified
into group A (carcinogenic to humans).
EPA has set an enforceable regulation for polychlorinated biphenyls, called a maxi-
mum contaminant level MCL, at 0.0005 mg/dm3 (EPA 1992b). The European Council
Directive 98/83/EC sets the standards for pesticides at 0.0001 mg/dm3, and pesticides
total at 0.0005 mg/dm3 (EU 1998). The polychlorinated biphenyls are not regulated in
the directive.
The current standards for particular pesticide level in drinking water set by the
Polish Ministry of Health Care are consistent with the European regulations and
amounting to 0.1 μg/dm3 (0.0001 mg/dm3), and 0.0005 mg/dm3 for total pesticides
84 Chapter 8
level (MHC 2007). The regulation does not mention the permissible polychlori-
nated biphenyl level but the previously obligatory document specified 0.5 μg/dm3
(0.0005 mg/dm3) of polychlorinated biphenyls as a standard for the drinking water
(MHC 2000).
The dose–response relation assessment has been limited to oral exposure of the
people affected because ingestion was regarded as a crucial exposure pathway for the
PCBs and pesticides present in the water. Besides, the main aim of the work was just
to determine the contribution of the selected POP contaminants (PCBs and COPs)
present in the water intakes, to excess health effects among the local population con-
suming the water. Actually the so called Excess Lifetime Cancer Risk ELCR for can-
cer effects and the so called hazard quotient for non-cancer effects originating from
PCBs and COPs in water consumed was discussed.
Among the general population of the district concerned, children in different ages
and a population of women and men (composing the population of adults (j)) are dis-
tinguished. The structure of the population is shown in Table 24.
The population uses the municipal system of water supply, drawing water from the
three wells examined. The drawn water is treated at the water treatment station and
delivered by drinking water pipes to customers.
As the contaminants concerned are suspected to produce both toxic (non-carcino-
genic) and carcinogenic adverse health effects, the dose–health response relation
was determined for both types of effects, on the basis of the available toxicity data.
Table 25 shows the characteristics of the monitored POPs: RfD, NOAEL – for toxic
effects and SFo, and carcinogen classification, according to (EPA 1986a) – for car-
cinogenicity.
Determination of dose–response relation is conducted separately for carcinogenic
and non-carcinogenic effects caused by the POPs absorbed from water.
Table 24. Structure of general population in absolute numbers and in %

(GUS 2004)
Population ( j)
1 2 3 4 5 6
Children Children Adults Men Women General
0–6 years old 7–17 years old (4 + 5) population
934 2046 8140 4192 3948 11120
8.4% 18.4% 73.2% 37.7% 35.5% 100%
Table 25. Carcinogenic classification, SFo values and toxicity of monitored POPs,
according to EPA, IRIS (EPA 1986a; OEHHA 2006)
U.S. EPA SFo

RfD NOAEL
Pollutant Carcinogens (mg/(kgday))–1
mg/(kgday) mg/(kgday)
IARC IRIS
0.007
∑ PCBs B2, Probable 2.0* 210–5
(Aroclor 1016)
1.10E+00 310–4
HCH 0.33
(RAIS) (gamma HCH)
DDE B2, Probable 3.40E–01 310–3
DDD B2, Probable 2.40E–01 910–3
DDT B2, Probable 3.40E–01 510–4 0.05
* Central-estimate slope factor (IRIS b) for high risk and persistence was applied for safety reason.
8.5. Dose–carcinogenic response relation
Because of the differential ability of different PCB mixtures to cause cancer, U.S.
EPA developed a range of cancer slope factors based on Aroclors 1016, 1242, 1254,
and 1260. These include the range of typical congeners found in various environ-
mental media such as water and fish (OEHHA 2006). In Table 25 the cancer potency
of PCB mixture is given (IRIS 1997).
For the carcinogenic effects the health risk was estimated using the formula (32). It
is valid for higher risk levels (i.e., above estimated risks of 0.01). For lower risks the
simpler, linear formula can be used (ELCR = LADD  CSF). Actually, in the present
work, the so called excess cancer risk over a lifetime ELCR, produced by oral intake
of PCBs and COPs with water has been determined instead of the general risk.
“Excess” means that additional cancer risk cases in the population are calculated,
which should be totaled up with the background risk to get absolute cancer risk. This
approach mathematically calculates the probability of developing cancer over a per-
son’s lifetime at a given exposure level. It is expressed by a value representing the
number of extra cancer cases expected in a given number of people on exposure to
a carcinogen at a stated dose. The ELCR concept was developed by the (EPA 1986a,
ENSR 2005). For the present case
ELCR = 1 – e–(LADD  CSFo) (32)
where:
LADD – lifetime average daily dose or intake of a pollutant with drinking water
averaged over the lifetime [mg/(kg body weightday)–1],
CSFo – an oral cancer slope factor [(mg/(kgday))–1].
86 Chapter 8
The ELCR value expresses the probability of an extra cancer case, e.g. 110–6
means one extra cancer case per one million people.
In the case of exposure to several carcinogenic substances, what is the case in the
present study, the total risk is assessed in accordance with the principle of the cumula-
tive effect of carcinogens on the body, by adding the risks calculated for the individual
carcinogens:
m
ELCR tot   ELCR
i 1
i
(33)
where:
ELCRtot – the total excess risk of occurrence of carcinogenic effects, caused by all
the substances.
ELCRi – the excess risk assessed for the i-th substance.
8.6. Dose–non-carcinogenic response relation
In case of the toxic, non-carcinogenic effects caused by the PCBs and COPs, not
risk but hazard quotient HQ was determined, for which the formula (34) is applicable.
As stated earlier in this book, the HQ has nothing to do with the risk. HQ is calculated
by comparing the average daily doses ADD of a pollutant taken in, with the reference
doses RfD.
HQ = ADD/RfD (34)
The ADD – exposure level (intake) expressed in mgkg–1day–1 is calculated differ-

ently, depending on the exposure durations. For the lifetime period it is equivalent to
the lifetime average daily dose LADD. For shorter durations appropriate averaging
times, not the lifetime, must be used. Also reference dose RfDs have to be consistent
with the exposure duration which means that the used RfD values should be deter-
mined for appropriate exposure periods.
For exposure to multiple non-carcinogenic substances, the aggregate potential for
the non-carcinogenic health effects – the hazard index HI was calculated from the
formula (35).
HI = Σ HQi (35)
The aim of this step of the health risk assessment is to quantify exposure to the
analyzed PCBs and COPs. It means that the taken in doses will be determined in com-
pliance with the assumed resident’s scenario. As the chemicals considered demon-
strate both toxic and carcinogenic effects, the quantification is conducted separately
for both effects. Since it is mainly the inhabitants using the water supply system who
are exposed to PCBs and COPs found in the water intakes, potential health effects
assessment was limited to the resident scenario. The particular populations and the
general population shown in Table 24 are exposed to the pollutants (i) present in
drinking water. The exposure path is the intake of the pollutants through the alimen-
tary tract.
The EPA Guidance for Superfund advises the upper-bound value of 30 years for
exposure duration (90-th percentile at one residence) when calculating maximum resi-
dential exposures MRE. In some cases, lifetime exposure, that is 70 years by conven-
tion, may be a more appropriate assumption (EPA 1989). Thus, the exposure durations
for all sub-populations considered and for carcinogenic and non-carcinogenic effects
will be as shown in Table 26.
Table 26. Exposure durations and averaging times for carcinogenic

and non-carcinogenic effects within the sub-populations, for the resident’s scenario
Children Children
Population: Adults
0–6 7–17
carcinogenic effects
Exposure duration (ED) – years 6 11 30
Averaging time (AT ) – days 25 550 25 550 25 550
non-carcinogenic effects
Exposure duration (ED) – years 6 11 30
Averaging time (AT ) – days 2 190 4 015 10 950
8.8. Exposure assessment for carcinogenic effects
For carcinogenic effects and the resident’s scenario the lifetime average daily dose
LADD can be calculated from relation derived from formula (36) (EPA 1992, Božek
2009):
LADD = c  FI  (IR  EF  ED)/(BW  AT) [mg . kg–1 . d–1] (36)

88 Chapter 8
where:
c represents the average concentration of polychlorinated biphenyls and organo-
chlorine pesticides in the wells during the monitoring period [ng/dm3];
FI (fraction ingested) is an absolute number in a range of 0–1, specifying the con-
tribution of the particular pollution sources to the pollutant intake by people. Accord-
ing to estimations made on the basis of data of the Food Surveys Research Group
(Sebastian et al. 2011), about 65% of the consumed water is plain tap water. The re-
maining 35% is bottled water. Similar proportion was applied in the present work,
thus, the FI was assumed 0.65;
IR represents the intake rate of the specific medium (water). For the particular age
groups the daily water intake rates according to (ECETOC 2001) are as follows: 0–6:
0.3 dm3/d, 7–17: 1 dm3/d, adults: 1.4 dm3/d;
EF is the exposure frequency = 365 days/year;
ED – the exposure duration. It depends on the age group and for the children from
group 0–6 it is 6 years, for the 7–17 group it is 11 years. For adults the upper-bound
value of 30 years was applied for the lifetime period, as recommended by (EPA 1989);
BW – the average body weight of 15 kg for the 0–6 age group, 46 kg for the 7–17
age group and 70 kg for adults (average) (EPA 1989);
AT – the averaging time = 70 years  365 days/year = 25 550 days for all age
groups. The AT was applied according to Superfund guidelines but some authors sug-
gest to apply the averaging times equal to exposure durations, when concentrations are
approximately constant in considered period of time (Božek et al. 2009). In such case
the calculated risks are significantly higher. The shorter the exposure period, the big-
ger differences exist between calculated values among the both approaches.
The calculated LADDs are shown in Table 27, as a matrix A of type m  n, where
m, n 0 ù, whose elements are doses taken in with water through the alimentary tract.
In aij the matrix elements, index i represents the type of a pollutant while index j rep-
resents a population distinguished from the general population. The LADD values are
valid for the resident scenario for which expose durations and averaging time are
given in Table 26.
Table 27. Individual lifetime average daily doses (LADD) of PCBs and COPs,
taken in by individuals in different populations
calculated from formula (36) [mg . kg–1 . d–1]
Pollutants LADD0–6 LADD7–17 LADDAdult

polychlorinated biphenyls 5.04E–07 1.00E–06 2.52E–06
gamma-Hexachlorocyclohexane (gamma-HCH) 6.21E–08 1.24E–07 3.11E–07
p, p-Dichlorodiphenyldichloroethylene (DDE) 4.10E–09 8.18E–09 2.05E–08
p, p-Dichlorodiphenyl dichloroethane (DDD) 6.68E–09 1.33E–08 3.34E–08
p, p-Dichlorodiphenyltrichloroethane (DDT) 9.04E–09 1.80E–08 4.52E–08
8.9. Exposure assessment for non-carcinogenic effects
For calculations of non-carcinogenic chemicals intakes for resident’s scenario the

same formula (37) is used, but instead of the lifetime average daily doses, average
daily doses ADD are determined.
ADD = c  FI  (IR  EF  ED)/(BW  AT ) [mg  kg–1  d–1] (37)
where particular symbols have the same meaning as in preceding formula (36) but
some have different value from these used for calculating LADD. In the case of
ADD the exposure duration ED value depends on the age group. For children from
group 0–6 it is 6 years and for the 7–17 group it is 11 years. For adults exposure dura-
tion AD = 30 years.
The values of averaging times AT equal the exposure durations and depend on
the age group. They are expressed in days. For the 0–6 age group AT0–6 = 2190,
AT7-17 = 4015 and for adults ATA = 10 950 days.
The calculated average daily doses ADD are shown in Table 28. The ADD values
are valid for the resident scenario for which expose durations and averaging times are
given in Table 26.
Table 28. Individual average daily doses ADD of PCBs and COPs,
taken in by individuals in different populations calculated from formula (37) [mg  kg–1  d–1]
Pollutant ADD0–6 ADD7–17 ADDAdult

PCBs 5.875E–06 6.386E–06 5.875E–06
Pollutant ADD0–6 ADD7–17 ADDAdult
COPs 5.875E–06 6.386E–06 5.875E–06
Quantification of the impact of considered water pollutants on the residents’ health

has been carried out on the basis of the absorbed doses, separately for carcinogenic
90 Chapter 8
and toxic effects. The calculated health risk levels related to carcinogenic effects and
comparison of the average daily doses with reference doses in case of toxic effects
enabled to determine the health threat level, the population is facing in the area oper-
ated by the local water system supply.
8.10.1. Cancer risk characterization
Table 29 shows excess lifetime cancer risks ELCR separately for the individual
pollutants and populations and the total risk for all the pollutants, occurring in the
particular populations, calculated from formulas (32) and (33). The total risk repre-
sents the total probability of cancer incidence above the natural level in the environ-
ment devoid of the investigated pollutants.
Table 29. ELCRind – i values resulting from individual pollutants,

calculated from equation (32) for particular populations, and ELCRtot – j
values resulting from cumulative effect of all pollutants,
calculated from equation (33) for particular populations
Pollutant ELCR0–6 ELCR7–17 ELCRA

ELCRtot – j
∑ELCR 1.171E–06 2.333E–06 5.855E–06
A comparison of the values shown in Table 29 with the unconditionally acceptable

ones shows that the highest carcinogenic risk is connected with the presence of PCBs
and HCH in water. In all the populations the total risk exceeds, although slightly, the
level of acceptable risk. In relation to the unconditionally acceptable risk level,
ELCRtot – j slightly exceeds safety standards in 0–6-children population, 2.3 times in
7–17-children population, and 5.8 times in adults’ population.
An individual risk can be converted into a population risk, i.e. into the expected
absolute number of extra cancer cases in the considered j-th population having size Nj
(Biesiada 2003).
ELCR pop  j  ELCR ind  j  N j (38)
where:
ELCRpop – j – a population excess cancer risk expressed as the total number of ex-
cess cancer cases in population j (children 0–6, children 7–19, women,
men, adults, general population, etc.), caused by a pollutant.
ELCRind – j – an individual excess cancer risk caused by a pollutant.
Nj – the number of people in the j population.
Each ELCRpop – j value is calculated separately for each of the pollutants.
The conversion of an individual risk into a population risk makes sense only for
appropriately large populations (in accordance with the law of larger numbers).
Table 30 shows ELCR for all the four populations (formula (38)): children 0–6,
children 7–17 and adults, as an absolute number of extra cancer cases in a given
population, due to the presence of a given pollutant. Also the total number of extra
cancer cases ∑ELCRpop caused by all the substances is shown. The expected absolute
number of extra cancer cases in the whole studied population ELCRgen – pop, due to the
contamination of water with all the pollutants amounts to about 0.053.
Table 30. ELCRpop – j values equivalent to absolute number of excess cancer cases in population j,
due to individual pollutant (i), cumulative ELCR values as sum of ELCRpop – j
within population ∑ELCRpop and ELCRgen – pop equivalent to absolute number
of excess cancer cases in whole population
Population
Children Children
Pollutant Adults
0–6 7–17
ECCpop – 1 ECCpop – 2 ECCpop – 3
∑ECCpop 1.094E–03 4.774E–03 4.766E–02
ECCgen – pop = 5.34E–02
The total risks ELCRtot – j are compared with the acceptable risk. The acceptable
risk level is usually assumed in a range of 110–6 to 110–4 (EPA 1991). The EPA as-
sumes the unconditionally acceptable risk level below 10–6 (1:1 000 000) (EPA 1986b,
EPA 2005). A risk of 10–3 absolutely requires protective measures. In general, the
US EPA considers excess cancer risks that are below 1 chance in 1 000 000 (110–6 or
1E–06) to be so small as to be negligible, and risks above 1E–04 to be sufficiently
large that some sort of remediation is desirable. A comparison of the values with the
unconditionally acceptable ones (i.e. 1E–06) shows that the highest carcinogenic risk
occurs in the resident scenario for adult group. PCBs contributes most to the excess
cancer risk. It exceeds the value 110–6 in all sub-populations but this cannot be a rea-
92 Chapter 8
son for any major concern of residents. The total risks ELCRtot – j in the particular sub-
populations produced by all the contaminants together are slightly higher than those
coming from PCBs only. This means that the COPs contribution to the total excess
cancer risk is insignificant.
8.10.2. Characterization of non-cancerous

health effects chances
Table 31 shows a matrix of hazard quotients HQij due to the contamination of wa-
ter with PCBs and COPs, calculated for the particular sub-populations. Also a hazard
index for the sum of all the pollutants is given in the Table. The values were calcu-
lated from formulas (14) and (15) based on the average daily doses ADD (Table 28)
and reference doses RfD (Table 25).
Table 31. Hazard quotients HQij and a hazard index HIj

for the sum of all the pollutants in water
Population
Children Children
Pollutant Adults
0–6 7–17
HQij
HIj
PCBs + COPs
2.964E–01 3.222E–01 2.964E–01
According to Table 31, both the HQ and the HI connected with the water pollut-
ants are below unity. Thus it can be concluded that the pollutants do not cause harmful
non-carcinogenic health effects in the population.
When assessing the health risk to people, resulting from the presence of toxic and
carcinogenic pollutants in the environment, one should expect certain simplifications
and ambiguities, due to which the obtained results cannot be regarded as definite and
absolute. The ambiguities and the simplifications are due to the imperfection of the
chemical analyses, the simplifying assumptions and the incompleteness of the toxico-
logical data on the substances. The procedure presented here is based on the conserva-
tive approach to risk assessment, which tends rather to overestimate than underesti-
mate risk. The main factors contributing to assessment uncertainty are:
 The lack of routine and systematic data from the monitoring of water intakes,
which would cover polychlorinated biphenyls and pesticides analyses. It is not
known whether the concentrations of the pollutants in the water intakes will re-
main at a constant level over the whole lifetime of the individuals belonging to
a given population.
 The average pollutant concentrations for the three water intakes supplying the
inhabitants with water were used in the calculations, however, there are quite
significant differences between the water intakes.
 Because of the incomplete data for risk calculation, toxicological data not for
pure polychlorinated biphenyls, but for a mixture of congeners were used.
 There is no information on the number of persons in the investigated popula-
tion, who use other water sources, such as local intakes and water supply sys-
tems operated by other drinking water producing plants. For that reason an es-
timation was applied assuming that the fraction of the plain tap water ingested
was 65% of total water consumption. The calculations were limited only to the
ingested water without taking into account dermal contact of human body dur-
ing washing and during taking a bath.
 Because of the lack of data on the absorption coefficients of the considered car-
cinogenic substances, the coefficients were assumed to be equal to 1 for all the
compounds.
8.12. Conclusions
The investigations on the presence of persistent organic pollutants POP in the envi-
ronment showed quite high concentrations of polychlorinated biphenyls and organo-
chlorine pesticides in the drinking water intakes supplying one of the districts near the
city of Wrocław. The origin of the pollutants is unknown, but one can suppose that
despite the fact that their use had been banned several decades ago they still infiltrate
from the industrial and agricultural areas where they had accumulated, into the under-
ground waters.
Observation of the pollutants’ levels in the wells, made during the five sampling
months did not show any significant regularity or systematic fluctuations, so it was not
94 Chapter 8
possible to draw sensible conclusions about the seasonal concentration trends. Deduc-
tion on possible trends could be possible providing that systematic long term analyses
are carried out.
Although the concentrations of the pollutants do not exceed the values allowable
for drinking water, the carcinogenic risk assessment carried out for the district’s dif-
ferent populations and its general population shows an excess risk of cancer ELCR,
which in some cases exceeds the unconditionally acceptable level of 10–6. The greatest
hazard is connected with the presence of polychlorinated biphenyls in the environ-
ment, whereas the concentrations of 1,2,3,4,5,6-Hexachlorocyclohexane (gamma-HCH),
p, p-Dichlorodiphenyltrichloroethane (DDT), p, p-Dichlorodiphenyl dichloroethane
(DDD) and p, p-Dichlorodiphenyldichloroethylene (DDE) do not pose a risk which
could be a cause for concern.
As regards the risk of toxic effects, the calculated hazard quotient HQ and hazard
index HI values do not give cause for concern. Under the current toxicity standards,
the investigated water intakes are completely safe as regards non-carcinogenic health
effects.
It should be stressed, that in case of carcinogenic effects in all subpopulations, the
calculated values are valid for the EPA approach, that is for averaging times equal to
lifetime. When other authors approach is applied, e.g., (Božek et al. 2009), assuming
the averaging time equal to exposure time, much higher ELCR values are obtained,
particularly in 0–6 years children population. Also the expected absolute number of
extra cancer cases in the whole studied population ECCgen – pop is higher than that cal-
culated according to (EPA 1989). It amounts to about 0.091, while the ECCgen – pop
calculated in compliance with EPA rules is 0.053.
9. Asbestos in the ambient air
9.1. Background
Asbestos is a common name for minerals derived from the group of serpentines
and amphiboles composing hydrated calcium, magnesium and sodium silicates. The
group of serpentines includes only chrysotile. Other five ones out of the six types be-
long to the group of amphiboles; they are: crocidolite, amosite, tremolite, antophylite
and actinolite. Chrysotile (white asbestos), crocidolite (blue asbestos) and amosite
(brown asbestos) have the largest industrial application.
Asbestos has unique chemical and physical properties, such as the resistance to
high temperature, resistance to the influence of bases, acids, sea water etc. At the same
time it is soft and pliant and is characterized by high elasticity and mechanical resistance.
In the early years of the past century asbestos found application in over 1000 production
technologies and in about 3000 products. It was used in the production of textile products,
yarn, rope, sealing, and abrasive products, such as brake blocks, in hydroinsulation
such as the roofing paper, the floor tiles, as the filtration aid in brewing etc (Trefler
et al. 2004).
For many years asbestos was considered as strategic material used for military pur-
poses in pipe covering which insulated hot steam pipes, hot water lines and fuel lines in
submarines and on navy ships, and in the filters for the army gas-masks, tanks, shelters
and other structures. Nevertheless, it was mostly used in the building industry in the
form of asbestos-cement roofing, the so-called “eternit”, asbestos-cement boards, pipes
and other products. Such application brought about extreme accumulation of this mate-
rial that has to be neutralized in some reasonable way. The problem concerning asbestos
neutralization results from the vast amounts of the asbestos products installed in the
industrial, communal and military facilities. For instance during the period of several
years of the product application in Poland about 16 million tons of asbestos and asbestos
containing materials was accumulated (Kazan-Allen 2004).
The evidence concerning the asbestos carcinogenicity began to emerge in the six-
ties. It was reported that fibers embedded in lung tissue over time caused serious lung
96 Chapter 9
diseases. Thus, much interest arose among specialists involved in the environment
health risk assessment, in health effects resulted from exposure to asbestos. The big-
gest asbestos health hazard results from the erosion of the already installed, improp-
erly taken down or stored asbestos and the products that contain it.
The first bans on the use of the asbestos materials started in the eighties. The EU
members have been obliged to limit the application of asbestos since 1991. Nowadays
all European Union member states banned using and production of asbestos contain-
ing materials. At the same time asbestos concentration limits in air were introduced
into the European legislation and measures taken aiming at abatement of human expo-
sure to asbestos.
A lot of asbestos neutralization methods can be found in literature. The proposed
ideas comprise a collection of wastes in specially constructed storage yards, cementa-
tion, covering the asbestos constructions on site with protective preparations prevent-
ing the fibers from being released to the environment, destruction using thermal or
microwave treatment, etc. (ATON 2010; Block 1998; Debailleul 2002; Mirick 1993;
Pritchett 1997; Trefler et al. 2003; Zaremba et al. 2010).
The methods of abatement of human exposure to asbestos were also a subject of
study on asbestos decomposition with the use of phosphoric acid, accomplished in the
frame of governmental scientific grants carried out at the Wroclaw University of Sci-
ence and Technology (Pawełczyk et al. 2017, Pawełczyk 2009, Trefler et al. 2004).
The research and tests carried out resulted in a novel asbestos processing method into
useful products, registered as a patent application (Trefler et al. 2003).
According to WHO estimates, more than 107 000 people die each year from as-
bestos-related lung diseases: cancer, mesothelioma and asbestosis resulting from
occupational exposure (WHO 2010). Until recently no precise toxicological factors
were available that could be useful for determination of the health risk resulting
from the exposure to asbestos. The calculations are mainly based on the inhalation
unit risk and carcinogenic slope factors published by the OEHHA and US EPA
(OEHHA a, RAIS b). As the air analyses are mainly expressed in fibers counts per
cubic centimeter the risk is calculated based on the unit risk data. The latter are
available also in units of measure related to the number of fibers. On the other hand,
the asbestos carcinogenic slope factor is expressed in (mg  kg–1  day–1)–1. Thus, to
make the risk assessment calculations based on this parameter possible, asbestos
concentration in the examined air should be converted from f/m3 into mg/m3. This
involves some complications in calculations and additional uncertainty factor to risk
assessment evaluation.
The presented health risk assessment was carried out at the Wroclaw University of
science and Technology as a consequence of a scientific project granted by the Polish
Ministry of Science and Higher Education entitled Waste-free technology of asbestos
utilization. The goal of this study was to investigate the outdoor air quality in selected
towns and a comparison of the results to air purity standards with respect to asbestos
Asbestos in the ambient air 97
airborne particles. Based on the air analyses, an estimation of possible health risk,
expressed in lung cancer probability in selected populations exposed to asbestos, has
been carried out.
It should be emphasized that the obtained results have to be interpreted cautiously,
taking into account numerous conscious uncertainties made during the risk considera-
tions. They could not be avoided because of incomplete toxicity data, limited number
of laborious measurements, high costs as well as certain inevitable assumptions, dis-
cussed further. Nevertheless the obtained results made it possible to evaluate the
health risk levels expected at the considered sites and thus can be a point of departure
for further discussion and research.
The vast accumulation of asbestos and asbestos containing materials in the envi-
ronment constitutes a serious problem as the erosion of these materials have led to the
contamination of air with airborne particles, mainly respirable fibers. Also demolition
of constructions, transportation and improper handling caused the environment con-
tamination with this material. The asbestos structures produce suspended dust particles
and fibers that are inhaled by people and animals. Exposure to the fibers can develop
health effects of which the intensity depends on:
 concentration of asbestos fibers in the air,
 duration of the exposure period,
 frequency of the exposure,
 the size of the asbestos fibers inhaled,
 the time since the exposure started and
 type of asbestos fibers in the air.
Breathing very high levels of asbestos may result in a slow buildup of scar-like tis-
sue in the lungs and in the membrane that surrounds the lungs. The respirable fibers
that cause the most problems are the microscopic variety that are small enough to be
inhaled deeply into the lungs, having a length exceeding 5 m and diameter less than 3
m. Some studies report the fibers less than 1m in diameter and more than 8 m are
the most dangerous (Krakowiak et al. 2009).
There are two types of cancer caused by exposure to asbestos: cancer of the lung
tissue itself and mesothelioma, cancer of the membrane that surrounds the lung and
other internal organs (NCI 2011). The lung cancer and mesothelioma do not develop
straight away after the initial exposure. They appear after many years. Smoking,
combined with inhaled asbestos, greatly increases the risk of developing the disease
(RAIS b; Salvatore et al. 2006).
98 Chapter 9
It has been proved that different types of asbestos fibers vary in carcinogenic po-
tency relative to one another. It appears, for example, that the risk of mesothelioma is
greater with exposure to crocidolite than with amosite or chrysotile exposure alone.
Also differences in fiber size distribution may contribute at least as much to the ob-
served variation in risk as the fiber type itself does (ATSDR 2001; IRIS c).
Because of the above mentioned adverse health effects, airborne asbestos con-
centration limits were set by different governments. In respect to asbestos, the air
purity standards are chiefly expressed in number of fibers per cubic centimeter or
meter. It may be confusing that some standard values are given in milligrams per
cubic meter. This involves difficulties in calculations and interpretation of the
results. Such unit’s incompatibility comes out of different techniques usually
applied for the concentration measurements, which can produce the outcomes ei-
ther in fiber counts or in milligrams per air volume unit. Polish asbestos occupational
standards in the workplace limit the permissible fiber concentration to 1 mg/m3 of the
total dust containing chrysotile asbestos and 0.2 asbestos fibers in 1 cm3. For croci-
dolite asbestos, the respective values are 0.5 mg/m3 and 0.2 fibers in 1 cm3 (MLSP
2002).
The official standards for the municipal air have not been set in Poland but it was
generally agreed on the basis of literature data that 1000 fibers/m3 (0.001 fibers/cm3)
can be accepted as an upper concentration safety level. On the other hand, permissible
concentrations of asbestos in the air for certain periods of exposure were established
(ME 1998). For every 30 minutes of exposure it amounts to 2.350 mg/m3, for 24 hours
to 1000 mg/m3 while for 1 year to 250 mg/m3. The first and the third values can only
be used for computational purposes.
In the US, asbestos standards were changed in 1994. The new standard was strained
significantly. The permissible exposure level had been halved to 0.1 fibers/cm3 (8 hour
time weighted average) for any form of asbestos. Thus, the US standard became one
of the strictest in the world (LHC 1995).
On the other hand, there is no consistent, convincing evidence that ingested as-
bestos is hazardous. There is, therefore, no need to establish a maximum acceptable
concentration for asbestos in drinking water (ATSDR 2001).
Since non-carcinogenic effects caused by exposure to asbestos are not as evident

as in the case of the carcinogenic ones, health effect considerations were limited only
to the cancer risk resulting from the contact with the asbestos polluted environment.
According to the carcinogen classification, asbestos, CAS number: 1332-21-4, is in-
cluded into group A – Human Carcinogen (EPA 1986a) or into group 1 – Carcino-
genic to Humans (IARC). Tables 32 and 33 give toxicity values for asbestos.
Table 32. Toxicity data of asbestos according to Integrated Risk Information System (IRIS),
California Environmental Protection Agency (CALEPA)
and Nevada Division of Environmental Protection (NDEP)
(EPAb, OEHHAa, RAISb)
Oral Slope Factor Inhalation Slope Factor Inhalation Unit Risk Factor
Authority
(mg . kg–1 . day–1)–1 (mg . kg–1 . day–1)–1 per ( f /cm3)–1
IRIS 2.3E–1(a)
CALEPA 1.90E–4 2.20E+2 1.9(b)
2.3E–1(c)
NDEP
6.3(d)
(a)
This value of Inhalation Unit Risk Factor (URF) refers to a combination of lung cancer and meso-
thelioma model for the population;
(b)
CALEPA URF value was determined using mesothelioma incidence in non-smoking females only
for its derivation;
NDEP approach distinguishes between amphibole and chrysotile risks (Black et al. 2011):
(c)
Chrysotile URF;
(d)
Amphibole URF.
URF is defined as the upper-bound excess lifetime cancer risk resulting from con-
tinuous exposure to an agent, at a concentration of 1 f/cm3 in air. It means that if the
unit risk = 210–6 per f/cm3, 2 excess cancer cases (upper bound estimate) are expected
to develop per 1 000 000 people, if exposed daily for a lifetime to 1 fiber of asbestos
in 1 cubic centimeter of air (EPA 1986a).
Table 33. The estimated air concentrations which would result

in lifetime cancer risks of 10–4, 10–5 and 10–6
Risk Level Concentration

E–4 (1 in 10 000) 4E–4 f /cm3
E–5 (1 in 100 000) 4E–5 f /cm3
E–6 (1 in 1 000 000) 4E–6 f /cm3
According to the IRIS sources, the asbestos unit risk is based on fiber counts made
by phase contrast microscopy PCM. Thus, the unit risk value derived in compliance
with this approach should not be applied directly to measurements made by other
analytical techniques.
Different approach was used for the risk calculations from that applied for PCBs
and COPs in water. The excess lifetime cancer risk ELCR has been determined using
100 Chapter 9
chronic exposure concentrations EC, instead of the lifetime average doses LADD. This
approach also calculates the probability of developing cancer over a person’s lifetime
at a given exposure level, The result produced is similar, too. It is expressed by a value
representing the number of extra cancer cases expected in a given number of people,
on exposure to a carcinogen at a stated dose. ELCRs were calculated from (EPA
1989):
ELCR = EC  URF (39)
where:
EC – Chronic Exposure Concentration (averaged over a 70-year lifetime) [ f /cm3]
– for explanation see the next section,
URF – Unit Risk Factor for inhalation of asbestos [( f/cm3)–1].
For the risk assessment, US EPA IRIS unit risk factor of 0.23 per f/cm3 was ap-
plied. That value is consistent with the analyses of the air samples collected from the
sites considered as the unit risk factor can only be used when the air concentration
does not exceed 4E–2 fibers/ml. Above this concentration, the factor may differ from
the one stated previously (IRIS c). The measurement results obtained are lower than
the EPA’s critical concentration.
The exposure to asbestos airborne fibers depends on their concentration in the air
and the population’s age group. The fiber concentration in the air in each town was
analyzed after the repeated triple sampling: in the morning, afternoon and midnight.
The three measurements from each town are not sufficient to apply statistical data
processing. Nevertheless the obtained results provide information about some regu-
larities among the particular towns. The values differ significantly depending on the
site and sampling time. The lowest air pollution was observed in smaller towns (i.e.
141–269 f /m3 in Zgorzelec), while in bigger cities it was much higher. In Chorzów
and Łódź for instance, it ranged between 800 to 1300 f /m3. Absolutely the highest
values were measured in Ruda Śląska where the concentration reached almost
1700 f /m3. Generally the increased levels of the air pollution were observed dur-
ing the rush hours. On the other hand, from among the three times of measurement
taking, the lowest fibers concentration was observed in the early morning. However
more measurements would be needed to catch the time and value of a real maximum
concentration. Figure 12 presents the maximum observed concentrations at particu-
lar sites.
Generally, from among of 60 air samples taken, in 21 samples, that means in 35% the
fibers concentration was below 200 f /m3. Only in three spots it exceeded 1000 f /m3.
Fig. 12. Concentration of asbestos fibers measured in the ambient air

in different towns of the south-west Poland at different times of the day [ f /m3]
The presented health risk assessment was carried out for the residents’ and occu-
pational scenarios, that is for people who are exposed to the polluted air over 24
a day and 8 hours a day, respectively. Five age groups were considered in the resi-
dents’ scenario involving children and adults (0–<2 years, 2–<6 years, 6–<16 years,
16–<30 years and 30–<70 years) (Table 34). These are conventional age groups recom-
mended in the US EPA guidelines discriminating specific data for the groups (body
weight, ingestion rates, etc.). Many other age sub-population can also be considered
depending on exposure scenarios and living habits.
Table 34. Population age division and exposure duration applied for risk assessment
in residents’ and occupational scenarios
Scenario Age range [years] Exposure duration [years]

0–<2 2
2–<6 6
Residents 6–<16 16
16–<30 30
30–<70 70
Employees 18–<55 37
One should stress that in order to observe conformity of the applied asbestos car-
cinogenic potency, expressed here as URF, with EPA risk assessment approach, the
70-year averaging time (AT) must be used in all calculations. This is because the URF
was determined based on 70-year lifetime (EPA 1991a). There are variety resident
exposure scenarios possible assuming not continuous stay at the place of living. Fre-
quent departures to school or to workplace are highly common among residents. Thus,
102 Chapter 9
taking into consideration sub-populations of students, employees or other resident

groups would be advisable. However in such a case the amount of data would be dras-
tically bigger, therefore only resident population is considered that has been continu-
ously exposed to the airborne asbestos at the locations studied. One should be aware
however, that with this assumption the calculated risks are overestimated.
On the other hand, in the occupational scenario it was assumed that the exposure of
adult employees starts with the age of 18 and it ends at the age of 55. The number of
work days in a year applied was 220. The respective exposure duration for all the sub-
population groups and scenarios is given in Table 34.
Asbestos is reported not to be mutagenic so it is not necessary to apply age-
dependent adjustment factors (ADAF), for particular groups in the risk calculations. It
would be expected that entrainment of asbestos to the air depends, among other things,
on traffic intensity, wind speed and air humidity. It is obvious that the concentration is
minimal on rainy days. This work assumes that the entrained fibers’ concentrations
depend only on the traffic intensity not on the weather, as similar weather conditions
were chosen for sampling. It was also assumed that residents are present at the spots
for 24 hours/day.
For the health risk assessment involving URF values, the so called chronic con-
centrations (EC) have to be calculated. The following airborne asbestos inhalation
exposure algorithm was used to determine chronic concentrations exposing all the age
groups of receptors (Braun 2005; Lytle 2007).
EC = Ca  ET  EF  ED/AT (40)
where:
EC – Chronic Exposure Concentration (averaged over a 70-year lifetime)
[f/cm3].
Ca – Asbestos Concentration in fibers per cubic centimeter [f/cm3].
ET – Exposure Time [hours/day]. It is 24 hours a day in the case of the resi-
dents’ scenario and 8 hours a day in the occupational scenario.
EF – Exposure Frequency [days/year]. In the resident scenario it is 365 days
a year. In the occupational scenario it is (8 h/24 h)  220 days a year (220
work days in the year was assumed and adults only are considered).
ED – Exposure Duration [years]. The value of ED depends on the age group. For
the children from the 0–2 group it is 2 years, for the 2–6 group it is 6 years,
for the 6–16 group it is 16 years. For adults from the 16–30 group it is
30 years and from 30–70 group it is 70 years.
AT – Averaging Time = 24 hours/day  365 days/year  70 years (lifetime) =
613 200 hours.
The EC values calculated for the considered scenarios, age populations and sites
are given in Tables 35 and 36.
Table 35. The chronic exposure concentrations (EC) calculated for residents’ exposure,
using maximum and minimum fiber counts [ f /cm3]
EC0–2 EC2–6 EC6–16 EC16–30 EC30–70

Town
min max min max min min min max min max
Brzeg 4.3E–06 5.3E–06 1.3E–05 1.6E–05 3.5E–05 4.2E–05 6.5E–05 7.9E–05 1.5E–04 1.9E–04
Chorzów 2.7E–05 3.8E–05 8.2E–05 1.1E–04 2.2E–04 3.0E–04 4.1E–04 5.7E–04 9.6E–04 1.3E–03
Gliwice 1.5E–05 2.6E–05 4.4E–05 7.9E–05 1.2E–04 2.1E–04 2.2E–04 4.0E–04 5.2E–04 9.2E–04
Gorzów 4.9E–06 9.3E–06 1.5E–05 2.8E–05 3.9E–05 7.5E–05 7.4E–05 1.4E–04 1.7E–04 3.3E–04
Jelenia G. 4.3E–06 6.0E–06 1.3E–05 1.8E–05 3.4E–05 4.8E–05 6.4E–05 9.0E–05 1.5E–04 2.1E–04
Kalisz 7.8E–06 8.6E–06 2.3E–05 2.6E–05 6.2E–05 6.9E–05 1.2E–04 1.3E–04 2.7E–04 3.0E–04
Katowice 2.3E–05 2.5E–05 6.8E–05 7.5E–05 1.8E–04 2.0E–04 3.4E–04 3.8E–04 8.0E–04 8.8E–04
Kraków 5.0E–06 9.6E–06 1.5E–05 2.9E–05 4.0E–05 7.7E–05 7.5E–05 1.4E–04 1.7E–04 3.4E–04
Legnica 4.9E–06 6.3E–06 1.5E–05 1.9E–05 4.0E–05 5.0E–05 7.4E–05 9.4E–05 1.7E–04 2.2E–04
Leszno 4.6E–06 6.7E–06 1.4E–05 2.0E–05 3.7E–05 5.3E–05 6.9E–05 1.0E–04 1.6E–04 2.3E–04
Łódź 2.3E–05 2.9E–05 7.0E–05 8.8E–05 1.9E–04 2.3E–04 3.5E–04 4.4E–04 8.1E–04 1.0E–03
Nowy T. 6.8E–06 9.3E–06 2.0E–05 2.8E–05 5.4E–05 7.5E–05 1.0E–04 1.4E–04 2.4E–04 3.3E–04
Opole 4.4E–06 8.4E–06 1.3E–05 2.5E–05 3.5E–05 6.7E–05 6.6E–05 1.3E–04 1.6E–04 2.9E–04
Oświęcim 6.5E–06 1.4E–05 2.0E–05 4.1E–05 5.2E–05 1.1E–04 9.8E–05 2.1E–04 2.3E–04 4.8E–04
Poznań 1.5E–05 2.3E–05 4.5E–05 6.9E–05 1.2E–04 1.8E–04 2.3E–04 3.5E–04 5.3E–04 8.1E–04
Ruda Śl. 3.2E–05 4.8E–05 9.6E–05 1.4E–04 2.6E–04 3.9E–04 4.8E–04 7.2E–04 1.1E–03 1.7E–03
Wałbrzych 5.3E–06 1.1E–05 1.6E–05 3.2E–05 4.3E–05 8.4E–05 8.0E–05 1.6E–04 1.9E–04 3.7E–04
Wrocław 5.1E–06 6.7E–06 1.5E–05 2.0E–05 4.1E–05 5.3E–05 7.7E–05 1.0E–04 1.8E–04 2.3E–04
Zgorzelec 3.7E–06 5.1E–06 1.1E–05 1.5E–05 3.0E–05 4.0E–05 5.6E–05 7.6E–05 1.3E–04 1.8E–04
Zielona G. 4.0E–06 7.7E–06 1.2E–05 2.3E–05 3.2E–05 6.1E–05 6.0E–05 1.2E–04 1.4E–04 2.7E–04
Table 36. The chronic exposure concentrations (EC) calculated for occupational exposure,
using maximum and minimum fiber counts [ f /cm3]
EC18–55 EC18–55
Town Town
min max min max
Brzeg 1.61E–05 1.96E–05 Łódź 8.62E–05 1.09E–04
Chorzów 1.02E–04 1.40E–04 Nowy Targ 2.53E–05 3.46E–05
Gliwice 5.50E–05 9.79E–05 Opole 1.65E–05 3.11E–05
Gorzów 1.83E–05 3.46E–05 Oświęcim 2.42E–05 5.11E–05
Jelenia G. 1.59E–05 2.24E–05 Poznań 5.60E–05 8.55E–05
Kalisz 2.90E–05 3.21E–05 Ruda Śl. 1.19E–04 1.79E–04
Katowice 8.45E–05 9.31E–05 Wałbrzych 1.99E–05 3.91E–05
Kraków 1.85E–05 3.57E–05 Wrocław 1.90E–05 2.47E–05
Legnica 1.84E–05 2.34E–05 Zgorzelec 1.38E–05 1.88E–05
Leszno 1.71E–05 2.49E–05 Zielona G. 1.50E–05 2.86E–05
The above chronic exposure concentrations were then used to calculate excess
lifetime cancer risks for the four age groups of residents and employees exposed, us-
ing the formula (39).
104 Chapter 9
The ELCRs for the considered exposure scenarios, estimated using the Integrated
Risk Information System inhalation unit risk factor and maximum measured concen-
trations are presented in Fig. 13 and 14.
The calculated maximum ELCR values for children from age groups 0–2 and
2–6 years old are rather insignificant or moderate. For older age group, that is for
6–16 years old sub–population the maximum ELCR values exceed in many towns 1E–
05 but they can still be acceptable. Relatively high values may arouse a concern in case
of Chorzów, Gliwice, Katowice, Łódź and Ruda Śl., particularly when older children
and adults are taken into account. In general, the US EPA considers excess cancer risks
that are below 1 chance in 1 000 000 (110–6 or 1E–06) to be small enough to be
considered negligible, and risks above 1E–04 to be sufficiently large enough to desire
some sort of remediation. Excess cancer risks that range between 1E–06 and 1E–04 are
generally considered to be acceptable, according to EPA. The highest carcinogenic risk
occurs in the resident scenario for the both adults groups in the above mentioned towns
and generally the calculated risks are the lowest in smaller towns.
It should be stressed, that in almost all age populations the risks exceed the accept-
able level of 1E–06 but this cannot be the reason for any major concern of residents
and thus no special measures need to be taken. The calculations were carried out under
assumptions of maximum fibers concentrations but when the lowest concentrations are
applied, the obtained risks are smaller. Additionally it has been assumed, that the resi-
dents stay in the polluted area continuously, which results in overestimation of the
risk. Nevertheless, in the case of some areas, the situation has to be constantly moni-
tored. When the occupational scenario is considered, almost all values approach the
levels of around 1E–06 to 5E–06 which are indisputably safe.
Fig. 13. Excess lifetime cancer risks for the considered age groups and sites in the residents’ scenario
Fig. 14. Excess lifetime cancer risks for the considered sites in the occupational scenario
It should be emphasize, that in case of carcinogenic effects in all subpopulations,

the calculated values are valid for the EPA approach, that is for averaging times
equal to lifetime. When other authors approach is applied, e.g., (Božek et al. 2009),
assuming the averaging time equal to exposure time, much higher ELCR values are
obtained.
9.6. Uncertainty in risk assessment
Evaluation procedure of the health risk to people exposed to presence of asbestos

in the environment assumes certain simplifications and ambiguities, due to which the
obtained results cannot be regarded as definite and absolute. The procedure presented
here is based on the conservative approach to risk assessment, which rather tends to
overestimate than underestimate the risk. The main factors contributing to assessment
uncertainty are:
 The exposure parameters used in these risk calculations (hours/day, days/year) were
based on the assumption that the residents stay at all times in the area of their resi-
dence. It is also obvious that they remain a substantial period of time in their homes
where indoor concentrations are certainly different from the outside ones.
 It is obvious that the concentrations of the asbestos fibers in the air will not re-
main at a constant level over the whole lifetime of the individuals belonging to
a given population. They fluctuate throughout the day and are highest during the
rush hours. There are also uncertainties regarding the concentrations employed
106 Chapter 9
to determine the chronic exposure concentrations. First, the results must be in-
terpreted with caution, because the sampling conditions were certainly not uni-
form in regard to the weather conditions at all sampling sites. The concentra-
tions may vary significantly depending on the weather parameters, which can
lead to some uncertainty in the derived ELCRs.
 The minimum and maximum fiber concentrations measured for all sites were
used in the calculations, so the real risks should lie between the extreme values
presented in the graphs.
 An assumption was made for the scenario of residents who are exposed to the
measured pollutant continuously, regardless the fact that they certainly are used
to leaving the permanent residence for studying or work.
 No distinction between different types of asbestos fibers (chrysotile, crocidolite)
present in the air was made during the measurements which involve additional
uncertainty associated with differences in the health effects caused by these
kinds of asbestos.
 There is a lack of data related to confounding factors such as smoking habits of
the residents which could synergically increase the ELCRs calculated.
9.7. Conclusions
Although the concentrations of asbestos fibers in air did not exceed the threshold
value of 1000 fibers per m3, except in the three spots mentioned above, generally
agreed as an unofficial standard for the municipal air, the concentrations of the fibers
in the considered town centers were quite high.
It was proven that the exhibiting risks calculated for children between the age
of 0–2 only slightly exceeded 1E–06 but these values are generally considered to be
acceptable. The ELCR representing the lifetime mortality risk for lung cancer
among adult residents, which was estimated using the US EPA approach, was less
than 1E–04, except for the 70–year–old sub–population. In case of the latter, the
maximum calculated risk occurred in Chorzów and it was 3.04E–04. In fact the real
values should be lower since the maximum measured fiber concentrations were ap-
plied to the calculations.
The maximum occupational cancer risks calculated for all sites were between
4.32E–06 and 4.12E–05 while the minimum ones between 3.18E–06 to 2.73E–5.
According to the applied standards, these values have been classified to rather moder-
ate levels.
For all exposure scenarios based on the maximum concentrations, the estimated
Excess Lifetime Cancer Risks remained within, or they surpassed the conventional
risk levels recommended by the US EPA in risk characterization. The studies require
further sampling to confirm or exclude risk levels approaching 1E–04.
The conclusions of the cancer risk assessment must be interpreted with caution.
It is important to point out that there is no evidence of a safe threshold for the car-
cinogenic effects of asbestos since an increased cancer risk has been observed in
populations exposed to very low concentrations of asbestos fibers. Taking that into
consideration, it is recommended to reduce the exposure as much as possible.
10. Summary
The presented case studies concern toxic and mutagenic substances found in the
soil, waters and air. The performed study concerned actual cases which included dif-
ferent autonomous projects carried out on various contaminated sites. This gave the
opportunity to investigate diverse health hazard conditions and environmental condi-
tions as well as different exposure scenarios. The pollution instances were a conse-
quence of emissions from running manufacturing processes, from accumulated waste
materials and from routine everyday populations activities.
The most important aim of the study was verification of the health risk assessment
procedures with regard to real situations where the environmental hazards might affect
population’s health. That means instances when simultaneously three factors exist, i.
e. the exposure source, the pathway and the receptor (Fig. 15).
Fig. 15. Unconditioned components of the health risk
In the case of occupational risk at the railway service station it was found that ex-
cess lifetime cancer risk is negligible. Cumulative for the mostly exposed worker’s
group, that is for the age group 60-64 years and full-shift exposure is about 7-fold
lower than the acceptable risk (ELCR = 10–6).
110 Chapter 10
The non-carcinogenic hazard level expressed in hazard quotients HQs and hazard
index HI for the all pollutants concerned are very low, as well.
As chromium emissions from the waste dump is concerned it was shown that quite
high concentrations of its trivalent and hexavalent forms were found in the environ-
ment. The level of non-carcinogenic hazards determined for the residents’ scenario
does not arouse any concern both for adults and children. The situation is completely
different in the case of the occupational exposure scenario concerning the waste proc-
essing. The calculated carcinogenic risk is extremely high for the workers, which im-
plies the necessity of careful revision of all unit operations included in the waste proc-
essing line in respect to hazard reduction.
The evaluation of health effects related to nitrate(V) and nitrate(III) in water has
shown that the levels of these compounds meet water purity standards.
As regards the risk of toxic effects, the calculated hazard quotients HQ and hazard
indexes HI do not give a cause for concern, however the HI could approach critical
unity value in case of an increase in community water consumption instead of bottled
water. For that reason it is not recommended to consider the river as a prospective
municipal water source, unless its purity standard is improved.
The investigations on the presence of persistent organic pollutants POP in drinking
water wells showed quite high concentrations of polychlorinated biphenyls and organo-
chlorine pesticides in the water intakes supplying one of the town in South West Poland.
Although the concentrations of the pollutants do not exceed the values allowable for
drinking water, the carcinogenic risk assessment carried out for the district’s different
populations shows an excess risk of cancer. As regards the toxic effects, the calculated
hazard quotients HQ and hazard index HI values do not give cause for concern.
The last case concerns asbestos fibers in the ambient air. Although the concentra-
tions of the fibers in the air, except in the three spots, did not exceed the threshold
value of 1000 fibers per m3 the concentrations of the fibers in the considered town
centers were quite high.
It was proven that the risks calculated for children only slightly exceeded 1E–06
but these values are generally considered to be acceptable. The ELCR among adult
residents, was less than 1E–04, The maximum calculated risk found in one spot was
3.04E–04. In fact the real risk values should be lower since the maximum measured
fiber concentrations were applied to the calculations.
The maximum occupational risks calculated for all sites were between 4.32E–06
and 4.12E–05 while the minimum ones between 3.18E–06 to 2.73E–5. According to
the applied standards, these values have been classified to rather moderate levels.
The presented health risk procedures may be used as some kind of model for or
other more or less similar cases. It is clear that any assessment should take into ac-
count individual character of the polluted area that means it should be taken into ac-
count type of contamination, actual exposure conditions, structure of the affected
population, their habits and other relevant factors.
References
Agency for Toxic Substances and Disease Registry, ATSDR (2001). Toxicological Profile for Asbestos,
September 2001, http://www.atsdr.cdc.gov/ToxProfiles/ tp61.pdf
Agency for Toxic Substances and Disease Registry ATSDR (2004). Toxicological Profile for Cobalt,
April 2004, http://www.atsdr.cdc.gov/toxprofiles/tp.asp? id=373&tid=64
Agency for Toxic Substances and Disease Registry ATSDR (2005). Public Health Assessment Guidance
Manual, 2005 Update, http://www.atsdr.cdc.gov/hac/ PHAManual/toc.html
Asbestos.com, (2014). Asbestos-Related Diseases and Smoking, http://www.asbestos.com/asbestos/
smoking/
ASHLEY K., FOOTE P., PERKINS J., WICKMAN D., (2003). NIOSH Manual of Analytical Methods (NMAM),
Fourth Edition. Method 7605, Issue 1.
ATON, (2014). Neutralization of asbestos waste, http://oferta.aton.com.pl/oferta/produkty/typoszereg-aton-ht/
aton-hr-a
BIESIADA M. (2000). Theory and practice of the health risk assessment, Environmental Medicine, 3(2),
83, pp. 29–37.
BILYK A., KOWAL A., (1993). Ocena stopnia zagrożenia terenów wodonośnych we Wrocławiu związkami
chromu, Ochr. Śr. (Environmental Pollution Control), No. 1–2, 3–6.
BLACK P., BALSHI M., PERONA R. (2011). Technical Guidance for the Calculation of Asbestos Related Risk in
Soils for the Basic Management Incorporated (BMI) Complex and Common Areas, NDEP Guidance for
Asbestos-Related Risk.
BLOCK J. (1998). Composition and method to remove asbestos, Pat. USA No. 5753031, 19.05.1998.
BOŽEK F., ADAMEC V., NAVRATIL J., KELLNER J., BUMBOVA A., DVORAK J. (2009). Health Risk Assess-
ment of Air Contamination Caused by Polycyclic Aromatic Hydrocarbons from Traffic. The 7th
WSEAS International Conference on Environment, Ecosystems and Development (EED ’09), Puerto
De La Cruz, Canary Islands, Spain, December 14–16, http://www.wseas.us/e-library/conferences/
2009/tenerife/ EED/EED-16.pdf
BOŽEK F., HUZLIK J., PAWEŁCZYK A., HOZA I., NAPLAVOVA M., JEDLICKA J. (2016). Polycyclic aromatic
hydrocarbon adsorption on selected solid particulate matter fractions, Atmospheric Environment,
ed. Elsevier, February 2016, Vol. 126, 128–135.
BRAUN R. (2005). Asbestos exposure and human health risk assessment, asbestos air sampling,
http://www.epa.gov/Region9/toxic/noa/clearcreek/pdf/ CCMA_HHRA TechMemo11-2004Sampling
_approval.pdf
BREBBIA C. A. (2010). Risk Analysis VII & Brownfields V, WIT Press, 2010, 924.
BROWNSON R.D., WARNER K.K., ROSENTHAL J.E. (2012). Current and Historical American Asbestos
Regulations, Brownson & Ballou, PLLP, Monaldi Archives for Chest Disease, 1998, Vol. 53, No. 2,
181–85, 2012 update.
CALLAHAN B. (2004). Review of the Army’s Technical Guides on Assessing and Managing Chemical
Hazards to Deployed Personnel, The National Academies Press, Washington, D.C., 2004.
112 References
ČÁSLAVSKÝ M., BOŽEK F., BUMBOVÁ A. (2010). Health risk analysis of the environmental burden. WIT
Transactions on Ecology and the Environment, Vol. 141, 135–144.
CHRISTOPHER Y., SEMPLE S., HUGHSON G.W., CHERRIE J.W. (2007). Inadvertent ingestion exposure in the
workplace, Institute for Occupational Medicine for the Health and Safety Executive 2007, Edinburgh,
https://www.google.pl/url?sa=t&rct=j&q=&esrc=s&source=web&cd=2&ved=0ahUKEwiuno3h4MTL
AhVkCpoKHeW1BGMQFggqMAE&url=http%3A%2F%2Fwww.hse.gov.uk%2Fresearch%2Frrpdf%
2Frr551.pdf&usg=AFQjCNFc6TojgqJp3iq1_m6nFCWRVlKvZw&sig2=rd_7GQgTp6zOAWdMG6IuN
Q&bvm=bv.116954456,d.bGg&cad=rja
COHEN B. (1996). Nitrate Contamination of Drinking Water, Environmental Working Group, February
1996, http://www.ewg.org/reports/nitrate
CONCHA-BARRIENTOS M., NELSON D., DRISCOLL T., STEENLAND N., PUNNETT L., FINGERHUT M., PRÜSS-
-ÜSTÜN A., AMES LEIGH J., WOO TAK S., CORVALAN C. (2004). Selected occupational risk factors,
Chapter 21 in: Comparative quantification of health risks, Edited by Majid Ezzati, Alan D. Lopez,
Anthony Rodgers and Christopher J.L. Murray, WHO Geneva, ISBN 92 4 158031 3, 2004.
CZECH T., BARAN A., WIECZOREK J. (2014). Zawartość metali ciężkich w glebach i roślinach z terenu
gminy Borzęcin (województwo małopolskie, Inżynieria Ekologiczna, DOI: 10.12912/2081139X.20),
nr 37, maj 2014, s. 89–98.
DAYAN A.D., PAINE A.J. (2001). Mechanisms of chromium toxicity, carcinogenicity and allergenicity:
review of the literature from 1985 to 2000. Hum. Exp. Toxicol., 20(9), 439–451.
DEBAILLEUL G. (2002). Process for the treatment of waste containing asbestos, Pat. USA No. 6391271,
21.05.2002.
DIANYI Y. (2008). Case studies in environmental medicine (CSEM), chromium toxicity. Agency for Toxic
Substances and Disease Registry (ATSDR), Clifton, GA, USA.
Dziennik Ustaw Dz.U. (2006). Rozporządzenie Ministra Środowiska z dnia 24 lipca 2006 r. w sprawie
warunków, jakie należy spełnić przy wprowadzaniu ścieków do wód lub do ziemi, oraz w sprawie
substancji szczególnie szkodliwych dla środowiska wodnego, Dz.U. z dnia 31 lipca 2006 r.
Dziennik Ustaw Dz.U. (2014). Rozporządzenie Ministra Pracy i Polityki Społecznej z dnia 6 czerwca
2014 r. w sprawie najwyższych dopuszczalnych stężeń i natężeń czynników szkodliwych dla zdrowia
w środowisku pracy, Dz.U. 2014, poz. 817.
ECETOC (2001). Exposure Factors Sourcebook for European Population, ECETOC, Brussels.
ENSR (2005). Remedial, Investigation/Feasibility Study Work Plan, Human Health Risk Assessment
Work Plan, ENSR Corp. Sept. 16, Vol. 5, Doc. No. 01776-020-156. http://www.epa.gov/region5/
sites/pines/pdfs/rifs200509/vol5-maintext.pdf
Environmental Protection Agency (EPA) (1986a). Risk Assessment for Carcinogens, http://www.epa.gov/
ttnatw01/toxsource/carcinogens.html
Environmental Protection Agency EPA (1986b). Guidelines for Human Health Risk Assessment of
Chemical Mixtures, Federal Register (51 FR 34014-34025) Washington D.C., downloaded from
http://cfpub.epa.gov/ncea/risk/recordisplay.cfm?deid=22567#Download
Environmental Protection Agency EPA (1989). Risk Assessment Guidance for Superfund, Vol. I. Human
Health Evaluation Manual, Part A, http://www.epa.gov/oswer/riskassessment/ragsa/pdf/rags-vol1-
pta_complete.pdf
Environmental Protection Agency EPA (1991). Risk Assessment Guidance for Superfund. Vol. I. Human
Health Evaluation Manual. Part B. Development of Risk-based Preliminary Remediation Goals.
Interim. EPA/540R-92/003. Publication 9285.7-01B. Office of Emergency and Remedial Response,
US Environmental Protection Agency, Washington, DC, USA.
Environmental Protection Agency EPA (1991a). Risk Assessment Guidance for Superfund, Vol. I, Human
Health Evaluation Manual, Supplemental Guidance “Standard Default Exposure Factors”, OSWER
Directive: 9285.6-03, March 25, 1991, http://rais.ornl.gov/documents/OSWERdirective9285.6-03.pdf
References 113
Environmental Protection Agency EPA (1992). Guidelines for exposure assessment, Federal Register,
57(104), 22888–22938, http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=15263#Download
Environmental Protection Agency EPA (1992b). Basic Information about Polychlorinated Biphenyls
(PCBs) in Drinking Water, http://water.epa.gov/drink/contaminants/basicinformation/polychlorinated
-biphenyls.cfm#four
Environmental Protection Agency EPA (1997). Exposure factors handbook. Washington, DC: Office of
Research and Development. EPA/600/P-95/002Fa,b,c.
Environmental Protection Agency EPA (1998). Toxicological review of trivalent chromium (CAS No.
16065-83-1) in Support of Summary Information on the Integrated Risk Information System (IRIS),
Washington, DC.
Environmental Protection Agency EPA (2004). Risk Assessment Guidance for Superfund. Volume I:
Human Health Evaluation Manual (Part E, Supplemental Guidance for Dermal Risk Assessment),
EPA/540/R/99/005 OSWER 9285.7-02EP PB99-963312 July 2004, http://www.epa.gov/oswer/
riskassessment/ ragse/pdf/introduction.pdf
Environmental Protection Agency EPA (2005). Guidelines for Carcinogen Risk Assessment, Washington, DC,
EPA/630/P-03/001FMarch 2005. http://www.epa. gov/raf/publications/pdfs/CANCER_GUIDELINES
_FINAL_3-25-05.PDF
Environmental Protection Agency EPA (2008). Child-Specific Exposure Factors Handbook (Final Re-
port) 2008, http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm? deid=199243
Environmental Protection Agency EPA (2009). EPA-540-R-070-002, OSWER 9285.7-82, January 2009,
Risk assessment guidance for superfund, Volume I: Human Health Evaluation Manual (Part F, Sup-
plemental Guidance for Inhalation Risk Assessment). Washington, DC.
Environmental Protection Agency EPA (2011a). 2011 Edition of the Drinking Water Standards and
Health Advisories. EPA 820-R-11-002, Washington, DC.
Environmental Protection Agency EPA (2011b). Exposure Factors Handbook: 2011 Edition EPA/600/
R-090/052F, September 2011, Washington, DC, http://water.epa.gov/action/advisories/drinking/upload/
dwstandards2011.pdf
Environmental Protection Agency EPA, (2011c). Exposure Assessment, http://cfpub.epa.gov/ncea/iris/
index.cfm?fuseaction=iris.showSubstanceList
Environmental Protection Agency EPA (2015). Chromated copper arsenate (CCA), http://www2.epa.gov/
ingredients-used-pesticide-products/chromated-copper-arsenate-cca
Environmental Protection Agency EPA (2015a). Basic information about chromium in drinking water,
http://water.epa.gov/drink/contaminants/basicinformation/ chromium.cfm#four
Environmental Protection Agency EPA (2015b). Integrated risk information system (IRIS), http://
cfpub.epa.gov/ncea/iris/index.cfm?fuseaction=iris.show Substance List
Environmental Protection Agency (2015c). Regional Removal Management Levels for Chemicals, Janu-
ary 2015, http://www.epa.gov/region4/superfund/programs/ riskassess/rml/rmlfaq.html
Environmental Protection Agency (2015d). Risk Communication, Attachment - 6: Useful Terms and
Definitions for Explaining Risk, http://www.google.pl/url?sa=t&rct=j&q=&esrc=s&source=web&cd
=2&cad=rja&uact=8&ved=0CC0QFjAB&url=http%3A%2F%2Fwww.epa.gov%2Fsuperfund%2F
community%2Fpdfs%2Ftoolkit%2Frisk_communication.pdf&ei=Be4wVbOUM5WwaZjigNgP&usg=
AFQjCNGGPHMYxF_dqR MjrbCsz5kEVKo 8sg&sig2=_2_YwC61ODtZENtrV-FPBA
Environmental Protection Agency EPA (2017a). Exposure Assessment, http://cfpub.epa.gov/ncea/iris/
index.cfm?fuseaction=iris.showSubstanceList
Environmental Protection Agency (2017 b). National Primary Drinking Water Regulations, http://
water.epa.gov/drink/contaminants/index.cfm
ESKENAZI B. (2006). DDT in Mothers Linked to Developmental Delays in Children, Science Daily, July 5.
European Union EU (1991). Nitrates Directive 91/676/EEC, http://ec.europa.eu/environment/water/water-
nitrates/index_en.html
114 References
European Union EU (1998). EU’s drinking water standards Council Directive 98/83/EC on the quality of
water indented for human consumption. Adopted by the Council, on 3 November 1998.
FALANDYSZ J., ISHIKAWA Y., NOMA Y., NAMASHITA N. (2007). Sklad chlorobifenyli w preparacie Chlo-
rofen w oparciu o rozdzial z użyciem fazy HT8-PCB Bromat. Chem. Toksykol., XL 2007, 4, 381–387.
FINLEY B., KERGER B., DODGE D., MEYERS S., RICHTER R. (1996). Assessment of airborne hexavalent chro-
mium in the home following use of contaminated tapwater, J. Expo. Anal. Environ. Epidemiol. Apr.–Jun.
6(2), 229–245.
FINLEY B., MONNOT A., PAUSTENBACH D., GAFFNEY S. (2012). Derivation of a chronic oral reference dose for
cobalt. Regul. Toxicol. Pharmacol. 2012 Dec., 64(3), 491–503, DOI: 10.1016/j.yrtph.2012.08.022.
FRANGOS J. (2011). Health risk assessment of hexavalent chromium release at Orica Kooragang Island,
Toxikos Report, TR200811-JF, Orica, Ltd., 28 Aug. 2011.
GAWĘDA E. (2014). Molibden i jego związki, Podstawy i Metody Oceny Środowiska Pracy, 2014,
nr 1(79), s. 131–140.
GRABAS K., KOŁWZAN B., PAWEŁCZYK A., BOŽEK F., STEININGER M. (2015). Bioremediation of Grounds
Contaminated with Petroleum Products by Heap Method, International Journal for Research in Applied
Science & EngineeringTechnology, ISSN: 2321-9653, Vol. 3, Issue X, October 2015, pp. 114–123.
GRINSVEN H. VAN, WARD M., NIGEL B., KOK T. DE (2006). Does the evidence about health risks associ-
ated with nitrate ingestion warrant an increase of the nitrate standard for drinking water?, Environ
Health, 2006, 5, 26.
GUERTIN J., AVAKIAN C., JACOBS J. (2004). Chromium(VI) Handbook, 1st Edition, CRC Press., ISBN:
978-1-56670-608-7, eBook ISBN: 978-0-203-48796-9.
GUS (Central Statistical Office) (2004). GUS Wrocław, September. Available at: http://www.google.pl/
url?sa=t&source=web&cd=2&sqi=2&ved=0CB0QFjAB&url=http%3A%2F%2Fwww.olesnica.wroc.
pl%2Fpliki%2Fbudownictwo%2Fprl%2Fplan_rozw_lokalnego.doc&rct=j&q=Plan%20Rozwoju%20
Lokalnego%20Gminy%20Ole%C5%9Bnica%202004-2006&ei=SRB0TcHeM8b5sgb25YiEDg&usg
=AFQjCNHH-m3TyXD9mcERBqJN00xtAAgrJA &sig2=jj75ql-WX9QfRvBzI8xuJ4g&cad=rja
HEATH J.S., KOBLIS K., SAGER S.H. (1993). Risk assessment for total petroleum hydrocarbons. Chapter 16.
In: Kostecki P., Calabrese E., eds. Hydrocarbon contaminated soils. Chelsea, MI, Lewis Publishers,
267–301.
HAYSE J.W., 2000, Using Monte Carlo Analysis in Ecological Risk Assessments, http://web.ead.anl.gov/
ecorisk/issue/pdf/montecarlo.pdf
HUTCHESON M.S., PEDERSEN D., ANASTAS N.D., FITZGERALD J., SILVERMAN D. (1996). Beyond TPH:
health-based evaluation of petroleum hydrocarbon exposures, Regul. Toxicol. Pharmacol., August 24,
1996, 1, Pt. 1, 85–101.
Instytut Uprawy, Nawożenia i Gleboznawstwa IUNG (1993). Wytyczne IUNG do oceny stopnia zanie-
czyszczenia gleb metalami ciężkimi, Puławy.
Integrated Risk Information Systems (IRIS) (1997). Polychlorinated biphenyls (PCBs) (CASRN 1336-36-3).
Database maintained by the Office of Health and Environmental Assessment. U.S. Environ-
mental Protection Agency, Environmental Criteria and Assessment Office, Cincinnati, Ohio,
http://www.epa.gov/iris/subst/0294. htm
Integrated Risk Information System IRIS, (2011), http://www.epa.gov/iris/subst/0371.htm
International Agency for Research on Cancer IARC, (2011). Agents Classified by the IARC Monographs,
Vol. 1–102, http://monographs.iarc.fr/ENG/Classification/ClassificationsAlpha Order.pdf. Cited 17 Aug.
2011.
JACOBS J., Testa S. (2004). Overview of chromium(VI) in the environment: background and history, by
CRC Press LLC, Chromium(VI) Handbook.
JAKUBOWSKI M. (2012). Podstawy i Metody Oceny Środowiska Pracy, 2012, nr 2(72), s. 111–146.
JAKUBOWSKI M., Ołów i jego związki nieorganiczne, z wyjątkiem arsenianu(V), ołowiu(II) i chromi-
anu(VI) ołowiu(II), Podstawy i Metody Oceny Środowiska Pracy, 2014, nr 2(80), s. 111–144.
References 115
KABATA-PENDIAS A. et al. (1993). Ocena stopnia zanieczyszczenia gleb i roślin metalami ciężkimi
i siarką. Ramowe wytyczne dla rolnictwa, IUNG, Puławy 1993.
KABATA-PENDIAS A., PIOTROWSKA M. (1995). Podstawy oceny chemicznego zanieczyszczenia gleb.
Metale ciężkie, siarka i WWA, Biblioteka Monitoringu Środowiska, PIOŚ, IUNG, Warszawa 1995, 28.
KELLY K.E. (1991). The Myth of 10-6 as a Definition of Acceptable Risk, 84th Annual Meeting, Air &
Waste Management Association, Vancouver, B.C., Canada, 16-21 June, 1991 http://www.google.pl/
url?sa=t&rct=j&q=&esrc=s&source=web&cd=4&cad=rja&uact=8&ved=0CD0QFjAD&url=http%3A%
2F%2Fnews.heartland.org%2Fsites%2Fall%2Fmodules%2Fcustom%2Fheartland_migration%2Ffiles%
2Fpdfs%2F17603.pdf&ei=kAkpVZafD9PcaJrHgsgD&usg=AFQjCNGIODXrfACJX6QGDKi_1i6max
7MvA&sig2=Kb6Fy_lBAQvQwHqNPBOTpA
KOOPMAN-ESSEBOOM C., HUISMAN M., WEISGLAS-KUPERUS N., BOERSMA E.R., DE RIDDER M.A.J.,
VAN DER PAAUW C.G., TUNSTRA L.G.M.T., SAUER P.J.J. (1994). Dioxin and PCB levels in blood and
human milk in relation to living areas in the Netherlands, Chemosphere, 1994, 29, 2327–2338.
KRAKOWIAK E., GÓRNY R., CEMBRZYŃSKA J., SĄKOL G., BOISSIER-DRAGHI M., ANCZYK E., (2009).
Environmental Exposure to Airborne Asbestos Fibres in a Highly Urbanized City, Annals of Agri-
cultural and Environmental Medicine, 2009, 16, 121–128.
LEBRECHT G., CZERCZAK S., SZYMCZAK W. (2003). Benzen, Podstawy i Metody Oceny Środowiska
Pracy, 2003, nr 1(35), s. 5–60.
LIGOCKA D. (2007). Ksylen – mieszanina izomerów, Podstawy i Metody Oceny Środowiska Pracy, 2007,
nr 4(54), s. 139–165.
London Hazards Centre LHC, (1995). Interchange Studios, The Asbestos Hazards Handbook,
http://www.lhc.org.uk/members/pubs/books/asbestos/asb_toc.htm
LYTLE G., WOO C. (2007). Asbestos Exposure and Human Health Risk Assessment, Asbestos Air Sam-
pling, EPA Region 9, Jere Johnson, WAM, Atlas Asbestos Mine Superfund Site, CCMA Human
Health Risk Assessment, September 5.
MACIEJEWSKI P., ŻUBER M., (2006). Prediction of contaminations after toxic industrial agent’s release
resulting from terrorist attacks, Natural and Civilization Disasters, Modern Terrorism, Political,
Social and Economical Aspects, Ed. by Marian Żuber, WSOWL, Wrocław, 189–202.
MILLS S.A., THAL D.I., BARNEY J. (2007). A summary of the 209 PCB congener nomenclature, Chemo-
sphere, 2007, Aug., 68(9), 1603–1612.
Ministry of Environment ME (2001). Poland, Decree 27.04.2001. Environmental Protection law, Dz.U.
(Journal of Laws of the Republic of Poland) No. 62, Item 627.
Ministry of Environment ME (2004). Poland, Decree 11.02.2004. on water classification, Dz.U. (Journal
of Laws of the Republic of Poland) No. 32, Item 284.
Ministry of Environment ME (2002). Poland, Decree from 9/09/2002 on Soil and earth quality standards,
Dz.U. (Journal of Laws of the Republic of Poland) No. 165, Item 1358 & 1359.
Ministry of Environment ME, (1998). Poland, Decree on Maximal Allowable Concentrations of Air
Polluting Substances Journal of Laws of the Republic of Poland, Dz.U. No. 55, Item 355, 28 April
1998.
Ministry of Environment ME, (2008). Poland, Decree on criteria and means of the evaluation of status of
underground waters, Dz.U. (Journal of Laws of the Republic of Poland) No. 143, Item 896, 23 July
2008.
Ministry of Health Care MHC (2007). Poland, Decree 29/03/2007 on requirements for water quality
intended for human consumption, Dz. U. (Journal of Laws of the Republic of Poland) No 61, Item 41.
Ministry of Health Care MHC (2000). Poland, Decree from 05/09/2000 on requirements for water quality
intended for human consumption, municipal and baths’ purposes, Dz.U. No. 82, Item 937.
Ministry of Health Care MHC (2007). Poland, Decree from 29/03/2007 on requirements for water quality
intended for human consumption, Dz.U. No. 61, Item 417.
116 References
Ministry of Health Care MHC, 2010. Poland, Decree 20/04/2010 on Requirements for water quality
intended for human consumption, Dz.U. (Journal of Laws of the Republic of Poland) No. 72.
Ministry of Labor and Social Policy MLSP, 2002. Decree 29/11/2002 on Maximal allowable occupational
concentrations. Dz. U. (Journal of Laws of the Republic of Poland) No. 217, Item 1833.
Ministry of Labor and Social Policy MLSP, (2002). Poland, Decree related to Maximal Allowable Con-
centrations and Intensity of Harmful Factors in Occupational Environment, Journal of Laws of the
Republic of Poland, Dz.U. No. 217, Item 1833, 29 Nov. 2002.
MIRICK W., FORRISTER W. (1993). Products for treating asbestos, Pat. USA, No. 5258131, 2.11.1993.
MOYA J., PHILLIPS L., SCHUDA L., CLICKNER R., BIRCH R., ADJEI N., BLOOD P., CHAPMAN K., CASTRO R.,
MAHAFFEY K., WOOD P., DIAZ A., LEE R. (2011). Exposure Factors Handbook, 2011 Edition, U.S.
Environmental Protection Agency Washington, EPA/600/R-090/052F.
National Cancer Institute NCI, (2011). Asbestos Exposure and Cancer Risk http://www.cancer.gov/cancertopics/
factsheet/Risk/asbestos
NHANES 2005–2008. Food Surveys Research Group Dietary Data Brief, No. 7, September 2011,
http://ars.usda.gov/Services/docs.htm?docid=19476
NAJBOROWSKI M., CHARAZIŃSKA S., LOCHYŃSKI P. (2017). Hazard and operability study (HAZOP) for
plant designed to crush big-bags with agglomerated fertilizer, Przem. Chem., 96/10, 2017, 2047–
2050, DOI: 10.15199/62.2017.10.2.
NISBET I.C.T., SAROFIM A.F. (1972). Rates and routes of transport of PCBs in the environment, Environ.
Health Perspect., 1972, 1, 21–38.
NOGAJ M. (2013). Hałda Solorza wreszcie zaczęła znikać, Gazeta Wyborcza Daily, Wroclaw, 28/10/2013.
Office of Environmental Health Hazard Assessment OEHHA (2006). Development of Guidance Tissue
Levels and Screening Values for Common Contaminants in California Sport Fish: Chlordane, DDTs,
Dieldrin, Methylmercury, PCBs, Selenium, and Toxaphene, http://oehha.ca.gov/fish/gtlsv/pdf/
draftgtlsvchddt.pdf
Office of Environmental Health Hazard Assessment OEHHA (2011). Hot Spots Unit Risk and Cancer
Potency Values, http://oehha.ca.gov/air/hot_ spots/ pdf/CPFs042909.pdf
OZE C., BIRD D., FENDORF S. (2007). Genesis of hexavalent chromium from natural sources in soil and
groundwater, P. Natl. Acad. Sci. USA (PNAS), 104(16), 6544–6549.
PAPP J.F. (2002). Mineral Yearbook 2002: Chromium. United States Geological Survey. Reston, VA.
PAUSTENBACH D., FINLEY B., MOWAT F., KERGER B. (2003). Human health risk and exposure assessment
of chromium(VI) in tap water, J. Toxicol. Environ. Health A, 66(14), 1295–1339.
PAWEŁCZYK A. (2008). Study on Removal of Nitrate Ions from Industrial Waste Waters by the Reduction
to Free Nitrogen, Environmental Pollution Control, Vol. 30, No. 4, pp. 45–48.
PAWEŁCZYK A. (2010). Environmental Health Risk Assessment of PCBs and Chlorinated Pesticides in
Drinking Water Intakes, 6-th International Scientific Conference on Natural and Civilization Disas-
ters – Dilemma of Modern Security, June 16–18, Slok, Poland.
Państwowy Instytut Geologiczny PIG (2016) – Polish Geological Institute (2016), unpublished report.
PAWEŁCZYK A., PRZĄDO D., STEININGER M. (2008). Research on PCB Contents in Selected Water Intakes
Located in Vicinity of City of Wrocław. In: Modern Chemical Technology in Agriculture and Envi-
ronment Protection, Ed. Czech-Pol, Prague, Vol. 9, pp. 256–261.
PAWEŁCZYK A., BOŽEK F., GRABAS K., CHĘCMANOWSKI J. (2017). Chemical Elimination of the Harmful
Properties of Asbestos from Military Facilities, Waste Management (Elmsford), 2017, Vol. 61, 377–385.
PAWEŁCZYK A., BOŽEK F., KOŁWZAN B., GRABAS K., STEININGER M. (2017a). Mitigation of the Envi-
ronmental Health Risk on Military Air Bases Polluted with Hydrocarbons, Journal of Environmental
Engineering, 2017, Vol. 143, No. 1, Item 05016007, 1–9.
Polish Standard PS (1982). PN-82/C-04576/08. Water and waste waters. Examination of nitrogen com-
pounds. Determination of nitrate nitrogen by the colorimetric method.
References 117
Polish Standard PS (1984). Protection of air purity. Air sampling. General guidelines for atmospheric air
sampling. PN-84/Z-04008.02.
Polish Standard PS (1988). Protection of air purity. Investigation of asbestos contents. Determination of num-
ber of respirable asbestos fibers on work stands by optical microscopy method. PN-88/Z-04202/02.
Polish Standard PS (1999). PN-EN 26777. Determination of nitrites by molecular absorption spec-
troscopy.
Polish Standard PS (2002). Poland, PN-EN ISO 6468:2002. Water quality – Determination of certain
organochlorine insecticides, polychlorinated biphenyls and chlorobenzenes – Gas chromatographic
method after liquid-liquid extraction.
PRITCHETT J., (1997). Method for abating bio-hazardous materials found in coatings, Pat. USA, No. 569812,
9.12.1997.
PROCTOR D., SUH M., MITTAL L., HIRSCH S., SALGADO R., BARTLETT CH., VAN LANDINGHAM C.,
ROHR A., CRUMP K. (2016). Inhalation cancer risk assessment of hexavalent chromium based on up-
dated mortality for Painesville chromate production workers, J. Expo. Sci. Env. Epid., 26, 224–231,
DOI: 10.1038/jes.2015.77.
Programme for Asbestos Abatement in Poland 2009–2032 (2010). Annex to the Resolution, No. 39/2010
of the Council of Ministers of 15 March 2010, Warsaw 2010.
PZWL (National Medical Publishing House) (1985). Kryteria Zdrowotne Srodowiska, Polichlorowane
Bifenyle i Terfenyle, Vol. 2, PZWL, Warsaw 1985.
Risk Assessment Information System RAIS (2011). Basic Information for Asbestos (in fibers),
http://rais.ornl.gov/tools/profile.php?analysis=Asbestos (in fibers)
SAIF Corporation (2009). Industrial hygiene hexavalent chromium. www.saif.com/_files/SafetyHealthGuides/
SS-835.pdf
SALVATORE C., SCHEFF P., SOKAS R. (2006). Determination of Asbestos Contamination in Beach Nourish-
ment Sand, Final Report of Findings, University of Illinois at Chicago, June 20.
SAPOTA A. (2002). Wielopierścieniowe węglowodory aromatyczne, Podstawy i Metody Oceny Śro-
dowiska Pracy, 2002, vol. 18, nr 2(32), s. 179–208.
SAPOTA A., DARAGÓ A. (2011). Kobalt i jego związki nieorganiczne, Podstawy i Metody Oceny Śro-
dowiska Pracy, 2011, nr 3(69), s. 47–94.
SEBASTIAN R.S., WILKINSON ENNS C., GOLDMAN J.D. (2011). Drinking Water Intake in the U.S.: What
We Eat In America, U.S. DEPARTMENT OF AGRICULTURE, Agricultural Research Service,
Beltsville Human Nutrition Research Center, Food Surveys Research Group, Dietary Data Brief,
No. 7, September 2011.
SEŃCZUK W. (2006). Toksykologia Współczesna, Medical Publishing House PZWL (ed.), Warsaw.
SNELL A., MILLS III, DAVID I. THAL, JONATHAN BARNEY (2007). A summary of the 209 PCB congener
nomenclature, Chemosphere, Vol. 68, Issue 9, August 2007, 1603–1612.
SOĆKO R., CZERCZAK S. (2010). Etylobenzen, Podstawy i Metody Oceny Środowiska Pracy, 2010,
nr 2(64), s. 109–130.
STAREK A. (1997). Polychlorinated biphenyls – Toxicology – Health Risk, Roczn. PZH, 1997, 48, No. 3, 205–316.
STAREK A. (2012). Styren, Podstawy i Metody Oceny Środowiska Pracy, 2012, nr 3(73), s. 101–135.
STAREK A., JAKUBOWSKI M. (2011). Miedź i jej związki nieorganiczne, Podstawy i Metody Oceny Śro-
dowiska Pracy, 2011, nr 2(68), s. 117–144.
SURGIEWICZ J. (2009). Chrom i jego związki, Podstawy i Metody Oceny Środowiska Pracy, 2009,
nr 1(59), s. 113–118.
SURGIEWICZ J. (2011). Bar i jego związki rozpuszczalne, In: Podstawy i Metody Oceny Środowiska
Pracy, 2011, nr 1(67), s. 29–34.
SWIAT J. (2012). Interpellation to the Ministry of Environment No 4703 on the matter of Siechnice waste
dump, http://www.sejm.gov.pl/sejm7.nsf/InterpelacjaTresc xsp? key=3282F4EB
118 References
SWIETLIK R. (1998). Speciation analysis of chromium in waters, Pol. J. Environ. Stud., 7(5), 257–266.
TODD G, CHESSIN R., COLMAN J. (1999). Toxicological Profile for Total Petroleum Hydrocarbons (TPH),
Agency for Toxic Substances and Disease Registry, Sept. 1999.
TREFLER B., PAWEŁCZYK A., NOWAK M. (2004). The Waste Free Method of Utilizing Asbestos and the
Products Containing Asbestos, Polish Journal of Chemical Technology, Vol. 6, No. 4, 56–59.
TREFLER B., PAWEŁCZYK A., ZWOŹDZIAK J., CZARNY A. (2003). Method of waste free utilization of as-
bestos and asbestos containing materials, Polish Pat. Appl., No. P-359958, 5.05.2003.
TULVE N.S., SUGGS J.C., MCCURDY T., COHEN HUBAL E.A., MOYA J. (2002). Frequency of mouthing
behavior in young children, J. Expo. Anal. Environ. Epidemiol., 12, 259–264, http://dx.doi.org/
10.1038/sj.jea.7500225.
World Health Organization WHO (2000). WHO Air Quality Guidelines for Europe, 2nd Ed., WHO Re-
gional Office for Europe, Copenhagen, ISBN 92 890 1358 3.
World Health Organization WHO (2014). Asbestos: elimination of asbestos-related diseases, http://
www.who.int/mediacentre/factsheets/fs343/en/
YUNG-TSE HUNG, LAWRENCE K. WANG, NAZIH K. SHAMMAS (2012). Handbook of Environment and
Waste Management: Air and Water Pollution Control, World Scientific Co., Pte., Ltd., New Jersey–
London–Singapore Beijing–Shanghai–Hong Kong–Taipei–Chennai, 2012, 1227.
ZAREMBA T., KRZĄKAŁA A., PIOTROWSKI J., GARCZORZ D. (2010). Study on the thermal decomposition of
chrysotile asbestos, Journal of Thermal Analysis and Calorimetry, Vol. 101, No. 2, 479–485.
ZAREMBA T., KRZĄKAŁA A., PIOTROWSKI J., GARCZORZ D. (2011). Investigations of Chrysotile Asbestos
Application for Sintered Ceramics Obtaining, Materiały Ceramiczne (Ceramic Materials), Vol. 63,
No. 1, 80–84.
List of Figures
Fig. 1. Sequence of the stages of the health risk assessment ........................................................... 10

Fig. 2. Threshold doses for toxic substances A, B and C ................................................................ 16
Fig. 3. Linear response to doses for carcinogenic substances X, Y and Z ...................................... 18
Fig. 4. Aerial view of the facility with the indicated ground and water sampling spots ................. 32
Fig. 5. Model of inadvertent ingestion exposure of hazardous substances in the soil (Christopher
et al. 2007) ........................................................................................................................... 46
Fig. 6. Comparison of hazard indices HI for exposure scenarios A, B, C and D (HI are the same
for both age groups) ............................................................................................................ 53
Fig. 7. Comparison of carcinogenic risks ELCR for exposure scenarios A, B, C and D for
workers’ age groups ............................................................................................................ 53
Fig. 8. Map of the area affected by the chromium waste dump with the indicated water sampling
spots .................................................................................................................................... 60
Fig. 9. Location of the chemical factory and sampling spot along the river ................................... 70
Fig. 10. Concentration of nitrate(V) in the river [mg/dm3] ............................................................... 71
Fig. 11. Concentration of nitrate(III) in the river [mg/dm3] .............................................................. 71
Fig. 12. Concentration of asbestos fibers measured in the ambient air in different towns of the
south-west Poland at different times of the day [ f /m3] ....................................................... 101
Fig. 13. Excess lifetime cancer risks for the considered age groups and sites in the residents’
scenario ............................................................................................................................... 104
Fig. 14. Excess lifetime cancer risks for the considered sites in the occupational scenario .............. 105
Fig. 15. Unconditioned components of the health risk ..................................................................... 109
List of Tables
Table 1. Parameters of chromatographic apparatus ........................................................................ 28

Table 2. Analyses of the soil with respect of metals and hydrocarbons concentration (gasolines,
mineral oils, BTEX, PAH) (PIG 2016) ............................................................................ 34
Table 3. Purity standards for C group soils [mg/kg d.m.] ............................................................... 36
Table 4. Limit values of trace metals in surface soil layer (0–20 cm) [mg/kg] .............................. 38
Table 5. Permissible contents of heavy metals 0–30 cm soil layer [mg/kg d.m.] ........................... 38
Table 6. Toxicity profiles of individual pollutants and maximum permissible concentrations
MPC [mg/m3] in the workplace ........................................................................................ 39
Table 7. Toxic parameters of the pollutants (EPA 2011c, ATSDR, IARC (International Agency
for Research on Cancer), RAIS) – the data concern oral expose route ............................. 43
Table 8. Daily doses in chronic toxic exposure (CDI) to individual pollutants in scenarios A, B, C
and D for extreme age groups of workers, that is 25–29 and 60–65 years [mg/(kg * d)] ..... 48
Table 9. Lifetime average daily doses in carcinogenic exposure (LADD) of individual pollutants
in scenarios A, B, C and D for extreme age groups 25–29 years and 60–64 years
[mg/(kg * d)] ..................................................................................................................... 49
Table 10. Hazard quotients HQ and hazard indices HI for the workers’ groups in the exposure
scenarios A, B, C and D ................................................................................................... 51
Table 11. Excess risks for individual carcinogenic pollutants ELCRi and total risks cancer ELCRt
calculated for the applied occupational exposure scenarios ............................................. 52
Table 12. Daily chromium intake doses by humans from different exposure routes (WHO 2000) ......... 58
Table 13. Contents of total and Cr(VI) in ground water collected from the piezometers (mg/L) ..... 63
Table 14. Contents of total and hexavalent chromium in the soil collected near the piezometers
(mg/kg) ............................................................................................................................. 63
Table 15. Contents of total and hexavalent chromium in the air collected from near the waste
processing plant (mg/m3) .................................................................................................. 63
Table 16. Carcinogenic and toxicity values of chromium (EPA 1992) ............................................ 65
Table 17. Hazard quotient HQi, hazard index HI and excess lifetime cancer risk (ELCR) ............... 67
Table 18. Toxicity of nitrates and nitrites related to methemoglobinemia as a critical health
effect (EPA 2017a) .................................................................................................. 74
Table 19. Child specific exposure factors applied for exposure quantification. Bottled water, bev-
erages and water included in purchased foods is not taken into account (EPA 2008) ...... 75
Table 20. Individual average daily doses ADD of nitrates and nitrites, taken in by all age sub-
populations absorbed by water ingestion and dermal contact [mg  kg–1  d–1] ................. 76
Table 21. Hazard quotients HQ and a hazard indexes HI for the children sub-populations ............. 77
Table 22. Qualitative and quantitative PCBs composition of water samples from three wells and
river [ng/dm3] ................................................................................................................... 82
Table 23. Organochlorine pesticides contents in water samples from three wells and river [ng/dm3] ..... 82
122 List of Tables
Table 24. Structure of general population in absolute numbers and in % (GUS 2004) .................................. 84
Table 25. Carcinogenic classification, SFo values and toxicity of monitored POPs, according to
EPA, IRIS (EPA 1986a, OEHHA 2006) .......................................................................... 85
Table 26. Exposure durations and averaging times for carcinogenic and non-carcinogenic effects
within the sub-populations, for the resident’s scenario ..................................................... 87
Table 27. Individual lifetime average daily doses (LADD) of PCBs and COPs, taken in by indi-
viduals in different populations calculated from formula (36) [mg  kg–1  d–1] ................ 88
Table 28. Individual average daily doses ADD of PCBs and COPs, taken in by individuals in dif-
ferent populations calculated from formula (37) [mg  kg–1  d–1] ..................................... 89
Table 29. ELCRind – i values resulting from individual pollutants, calculated from equation (32) for
particular populations, and ELCRtot – j values resulting from cumulative effect of all
pollutants, calculated from equation (33) for particular populations ................................ 90
Table 30. ELCRpop – j values equivalent to absolute number of excess cancer cases in population j,
due to individual pollutant (i), cumulative ELCR values as sum of ELCRpop – j within
population ∑ELCRpop and ELCRgen – pop equivalent to absolute number of excess cancer
cases in whole population ................................................................................................. 91
Table 31. Hazard quotients HQij and a hazard index HIj for the sum of all the pollutants in water ...... 92
Table 32. Toxicity data of asbestos according to Integrated Risk Information System (IRIS), Cali-
fornia Environmental Protection Agency (CALEPA) and Nevada Division of Environ-
mental Protection (NDEP) (EPAb, OEHHAa, RAISb) .................................................... 99
Table 33. The estimated air concentrations which would result in lifetime cancer risks of 10–4,
10–5 and 10-6 ..................................................................................................................... 99
Table 34. Population age division and exposure duration applied for risk assessment in residents’
and occupational scenarios ............................................................................................... 101
Table 35. The chronic exposure concentrations (EC) calculated for residents’ exposure, using
maximum and minimum fiber counts [ f /cm3] ................................................................. 103
Table 36. The chronic exposure concentrations (EC) calculated for occupational exposure, using
maximum and minimum fiber counts [ f /cm3] ................................................................. 103
About the Authors
Adam Pawełczyk, Ph.D., D.Sc. (Dr hab. inż.), is Assistant

Professor at Faculty of Chemistry, Wrocław University of
Science and Technology, Wroclaw, Poland. His primary re-
search interests are in the fields of assessment of environmental
health risk, risk abatement techniques, reclamation of chemical-
ly polluted environment, waste materials recycling and
processing into useful products. His research focus is
environment quality and his primary professional goal is to
apply engineering to maintain a high quality environment
in a wise and cost-efficient fashion. Dr hab. inż. Adam Pawełczyk Ph.D., D.Sc. earned
his Ph.D. in chemical technology and his habilitation in safety sciences. He has written
in professional journals and his book ”Environmental health risk and its sustainable
abatement”. He also published, as a co-author, a frequently cited handbook “Introduction
to Environmental Microbiology”. His articles and book chapters deal with environ-
mental pollution, abatement of health risk, waste utilization and waste processing into
useful products. He led numerous governmental and commercial projects on polluted
environment reclamation, waste materials processing and environmental impact of
chemical technologies.
František Božek, Prof. Ing., Ph.D., C.Sc. He graduated

from the University of Chemical Technology in Pardubice,
branch of study – Macromolecular Substances Technology.
After the graduation he was admitted to study for a post-
graduate degree of the Academy of Sciences of Czecho-
slovakia at the Macromolecular Chemistry Research Institute
in Brno. He dealt with the problems of ionic polymerization
of oxygen heterocyclic compounds. In 1979 he submitted his
dissertation and in 1988 he was appointed associate professor at
the University of Chemical Technology in Pardubice in the
branch called Macromolecular Chemistry. In 1993 he habilitated. In 1978 he started
working at the University of the Ground Forces where he was executing the duties of
124 About the Authors
vice-dean of research work for 6 years. In 2002 he was appointed for the post of pro-
fessor in the branch Force and Civil Protection. Since 1989 he has been dealing with
the problems of the environmental protection focused on waste management, proac-
tive tools of environmental policy and especially risk management, currently at the
University of Defence and the Mendel University of Agriculture and Forestry in Brno.
He is a member of pilot studies and working groups of NATO and US EPA, scientific
and branch councils and many foreign professional and scientific societies.
Marian Żuber, Ph.D., D.Sc. (Dr hab. inż.), is Professor

at Faculty of Security Studies of the Tadeusz Kosciuszko
Military University of Land Forces in Wrocław, Poland. His
primary research interests are in the fields of terrorism and
weapon of mass destruction, crisis management, ecological
threats, ecological security. He accomplished his Ph.D. in
environment engineering in Wrocław Technical University.
He is the author or co-author of numerous publications
connected with his field of scientific activity, for example:
Genetically Modified Food – course or Chance for Starvings?,
Former uranium mines as a source of higher level of ionising radiation, Systemic public
security management in cross-border crime, Zoonotic diseases as the agents in bioter-
rorism, Ricin – The potential bioterrorist agent, Agroterrorism – threats and prepar-
edness, Removal of Radioisotopes from Waste Water After “Dirty Bomb” Decon-
tamination. He has organized international conference series about natural and
civilization disasters.

Case Studies Important Environmental - Risk - v1

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Case Studies Important Environmental - Risk - v1

Uploaded by

Copyright:

Available Formats

Adam Pawełczyk

© Copyright by Adam Pawełczyk, Wrocław 2018

List of Abbreviations .......................................................................................................................... 5

7.7. Hazard characterization ....................................................................................................... 76

AD – Adults Exposure Duration

PCBs – Polychlorinated Biphenyls

dose-response relation, risk characterization and ending with uncertainty analysis.

The commonly accepted approach of environmental hazard assumes comparison of

Fig. 1. Sequence of the stages of the health risk assessment

2.2. Hazard identification

2.3. Exposure assessment

Exposure assessment consists in determining doses of particular chemicals ab-

Intake of chemicals by ingestion with drinking water

Intake of chemicals by inhalation with air

Intake of chemicals by ingestion of contaminated fruits and vegetables

Similar formula is applied for calculations of the chemicals intake by ingestion of

Intake of chemicals by accidental ingestion of contaminated soil

Absorbed dose of chemicals by dermal contact with the contaminated soil

Toxic (non-carcinogenic) chemicals

 longer term exposure to non-carcinogenic toxicants (developmental and acute)

2.4. Dose–response assessment

The dose–response assessment is a step in which toxicological and epidemiologi-

2.4.1. Toxic substances

Fig. 2. Threshold doses for toxic substances A, B and C

Fig. 3. Linear response to doses for carcinogenic substances X, Y and Z

Risk = CSF  CDI (10)

Risk = 1 – e–(CDICSF). (11)

2.5. Risk characterization

Risk characterization is an integral element of the risk assessment procedure for

2.6. Uncertainty analysis

Chromium in the soil

Polychlorinated biphenyls in water

Table 1. Parameters of chromatographic apparatus

Hydrocarbons in water and soil

environmental risk estimation on the contaminated area is based on guidelines pub-

5.2. The site characterization

The considered facility is a delimitated property which is a part of a bigger com-

Fig. 4. Aerial view of the facility with the indicated ground

5.3. Starting data

Table 2. Analyses of the soil with respect of metals and hydrocarbons

5.4. Hazard identification and toxicity assessment

Hazard identification was performer based on comparison soil chemical analyses,

Table 3. Purity standards for C group soils [mg/kg d.m.]*

Contaminant Soil group Concentration

However by using the sewages for fertilization, permissible concentration of heavy

Despite of relatively low environment contamination it is not known if a real

5.5. Toxicity profiles of the studied contaminants

Table 6. Toxicity profiles of individual pollutants

Table 7. Toxic parameters of the pollutants (EPA 2011c, ATSDR, IARC

NOAEL/*LOAEL RfD SForal Carcinogenicity

5.6. Exposure assessment

Fig. 5. Model of inadvertent ingestion exposure of hazardous substances in the soil

 model of occupational exposure by incidental soil ingestion by Christopher

Table 8. Daily doses in chronic toxic exposure (CDI) to individual pollutants

Doses in toxic exposure CDI

Table 9 shows the results of calculations of the doses in carcinogenic exposure

Table 9. Lifetime average daily doses in carcinogenic exposure (LADD)

Doses in toxic exposure CDI

5.7. Determination of dose–response relation

Determination of dose–response relation enables to assess health hazard quantita-

where HQi is a hazard quotient for the i-substance.

Table 10. Hazard quotients HQ and hazard indices HI

Hazard Quotient HQi