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ABSTRACT
THUNE, I., and A. S. FURBERG. Physical activity and cancer risk: dose-response and cancer, all sites and site-specific. Med. Sci. Sports
Exerc., Vol. 33, No. 6, Suppl., 2001, pp. S530 –S550. Purpose: The association between physical activity and overall and site-specific cancer
risk is elaborated in relation to whether any observed dose-response association between physical activity and cancer can be interpreted in
terms of how much physical activity (type, intensity, duration, frequency) is needed to influence site- and gender-specific cancer risk.
Methods: Observational studies were reviewed that have examined the independent effect of the volume of occupational physical activity
(OPA) and/or leisure time physical activity (LPA) on overall and site-specific cancer risk. Results: The evidence of cohort and case-control
studies suggests that both leisure time and occupational physical activity protect against overall cancer risk, with a graded dose-response
association suggested in both sexes. Confounding effects such as diet, body weight, and parity are often included as a covariate in the analyses,
with little influence on the observed associations. A crude graded inverse dose-response association was observed between physical activity
and colon cancer in 48 studies including 40,674 colon/colorectal cancer cases for both sexes. A dose-response effect of physical activity on
colon cancer risk was especially observed, when participation in activities of at least moderate activity (⬎4.5 MET) and demonstrated by
activities expressed as MET-hours per week. An observed inverse association with a dose-response relationship between physical activity and
breast cancer was also identified in the majority of the 41 studies including 108,031 breast cancer cases. The dose-response relationship was
in particular observed in case-control studies and supported by observations in cohort studies when participation in activities of at least
moderate activity (⬎4.5 MET) and demonstrated by activities expressed by MET-hours per week. This association between physical activity
and breast cancer risk is possibly dependent on age at exposure, age at diagnosis, menopausal status and other effect modifiers, e.g., body
mass index. Furthermore, data concerning carcinoma of other cancers (prostate, lung, endometrium, ovary, and testicular cancers) are required.
Conclusion: A protective effect of physical activity on site-specific cancer risk with a dose-response association between physical activity
and colon and pre- and postmenopausal breast cancer supported by identified biological mechanisms has been observed. The optimal
permutation of type, intensity, duration, and frequency of physical activity across the lifespan is unclear, but it is gender, age, and site specific
and supports moderate activity (⬎4.5 MET) more than light activities (⬍4.5 MET). The complicated nature of the physical activity variable,
combined with lack of knowledge regarding possible biological mechanisms operating between physical activity and cancer, warrants further
studies including controlled clinical randomized trials. Key Words: PHYSICAL ACTIVITY, CANCER RISK, BIOLOGICAL MECHA-
NISMS, DOSE-RESPONSE
E
nvironmental exposure has been accepted as a major mainly in the last decade that investigators, encouraged by the
causal factor of cancer (80 –90%) (67). Our genetic findings of animal studies, have linked physical activity to
constitution was selected for a lifestyle characterized by human cancer risk (101). This evidence comes from observa-
physical activity. People who have a sedentary Western life- tional studies, as no intervention studies so far have been
style in the year 2000 may be about 0.003% different geneti-
cally from late Stone Age people of 10,000 yr ago (104).
Consequently, a sedentary lifestyle may be one explanation for
the variation in cancer incidence rates and changes in incidence
rates observed in migration studies between and within coun-
tries and among subgroups of people.
Although Rammazzini 300 yr ago suggested that physical
activity played a role in human cancer etiology (95), it is
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MEDICINE & SCIENCE IN SPORTS & EXERCISE®
Copyright © 2001 by the American College of Sports Medicine
S530
TABLE 1. Studies on physical activity and overall cancer risk, dose-response.
Age at RR (95% CI) Highest vs Lowest Physical Activity Dose-Response
Follow-Up Baseline Physical Activity Evidence
Cohort Study Study Population Total (N) Time (yr) Cases (N) Assessment LPA OPA Total LPA OPA Total Category
Albanes et al., 1989 National Health and M 5141 7–13 25–74 M 460 Questionnaire (LPA, 0.5 (0.4–0.8) S C
USA (1) Nutrition Survey F 7407 F 399 OPA) 0.8 (0.6–1.3) NS
(Incidence)
Arraiz et al., 1992 Canada fitness M ⫹ F 42,239 7 30–69 165 (Fatal) Questionnaire (LPA, 0.8 (0.5–1.4) LPA NS C
Canada (4) survey OPA) 0.5 (0.2–1.3) Fitness
Fitness
Blair et al., 1989 Texas Cooper clinic M ⫹ F 13,344 8 20⫹ 82 (Fatal) Fitness—treadmill M: 0.2 S S C
USA (8) F: 0.2 S S
Chang-Claude et al., 1993 Vegetarian M ⫹ F 1904 11 ? 304 (Fatal) Questionnaire (LPA) 1.0 (0.3–3.0) NS C
S531
TABLE 2. Studies on physical activity and colorectal, colon, and rectal cancer risk, dose-response.
Age at
S532
RR (95% CI) Highest vs Lowest Physical Activity Dose-Response
Baseline Physical Activity Evidence
Cohort Studies Study Population Total (N) Follow-Up Time (yr) Cases (N) Assessment—Dose LPA OPA Total LPA OPA Total Category
Albanes et al., 1989 National Health and M 5138 7–13 25–74 62 CR Questionnaire 1.0 (0.5–2.0) CR 0.6 (0.3–1.4) CR NS NS C
USA (1) Nutrition Survey F 7407 66 CR Interview (LPA, OPA) 0.8 (0.4–1.7) CR 1.4 (0.5–3.3) CR NS NS
Ballard-Barbash et al., 1990 Framingham M 1906 28 30–62 73 CR Questionnaire 0.6 (0.3–1.0) CR — C
USA (5) F 2308 79 CR Physician Interview 0.9 (0.6–1.7) CR —
(LPA)
Bostick et al., 1994 Iowa F 3215 5 55–69 212 C Questionnaire 1.1 (0.7–1.5) C NS C
USA (9) Self-report (LPA)
Chow et al., 1993 Shanghai 1980–84 M ⫹ F 83,202 1980–84 All M 2291 C Occupational M: 0.8 (0.7–0.9) C S C
China (18) F 936 C Category (OPA) F: 0.9 (0.8–1.0) C S
Clemmesen, 1998 Copenhagen male M 5248 15 40–59 88 C Questionnaire (LPA) 0.5 (0.3–0.8) C S C
Denmark (19) Cohort 55 R 0.9 (0.4–2.0) R NS
Gerhardsson et al., 1986 Population M 1.1 million 19 20–64 5100 C Questionnaire 0.8 (0.7–0.9) C — C
Sweden (36) 4533 R Self-report Occupation (Prox) —
(OPA, LPA) 0.9 (0.8–1.0) R
Gerhardsson et al., 1988 Swedish twin M ⫹ F 164,777 14 42–81 M 99 C Questionnaire M ⫹ F: 0.3 (0.1–0.8) — C
Sweden (37) registry F 92 C Self-report (OPA, LPA)
Giovannucci et al., 1995 Health M 47,273 6 40–75 203 C Questionnaire 0.5 (0.3–0.9) C S C
USA (39) professionals Self-report (LPA)
Hsing et al., 1998 Lutheran M 17,633 20 Not stated 120 C Occupational title (OPA) 0.4 (0.2–0.9) C — C
USA (46) Brotherhood 25 R
Insurance
society
http://www.acsm-msse.org
TABLE 2. Continued
Sources of Physical Activity RR (95% CI) Highest vs Lowest Physical Activity Dose-Response Evidence
Case-Control Studies Study Population Controls Age (yr) Controls Cases N Assessment—Dose LPA OPA Total LPA OPA Total Category
Will et al., 1998 Population M 342,859 13 30⫹ 3218 CR Questionnaire M: 0.7 (0.6–0.9) — C
USA (132) Cancer prevention, F 510,850 4006 CR Self-report (LPA, OPA) CR
25 states F: 0.9 (0.8–1.1)
CR
Wu et al., 1987 Retirement cohort M⫹F 4.5 M 58 CR Questionnaire M: 0.4 (0.2–0.8) CR S C
USA (133) 11,888 F 68 CR Self-administered (LPA) F: 0.9 (0.5–1.6) CR NS
Arbman et al., 1993 Hospital Hospital and ⬍75 M⫹F M 51 C Occupational (OPA) 1.1 (0.6–2.0) C — C
Sweden (3) population 371 Hosp 48 R 2.1 (1.2–3.9) R —
registries 430 Pop F 47 C
31 R
Benito et al., 1990 Majorca Population ⬍80 M 295 M 72 C Questionnaire M ⫹ F: 0.7 S S C
Spain (6) F 203 73 R Self-report (OPA)
S533
S534
TABLE 2. Continued
Sources of Physical Activity RR (95% CI) Highest vs Lowest Physical Activity Dose-Response Evidence
Case-Control Studies Study Population Controls Age (yr) Controls Cases N Assessment—Dose LPA OPA Total LPA OPA Total Category
Peters et al., 1989 Cancer Registry Neighborhood ⬍45 M 147 147 C Questionnaire 0.9 (0.4–2.0) CR — C
USA (91) Los Angeles F 41 41 R Interview (OPA) 1.4 (0.4–5.0) R —
Slattery et al., 1988 Utah Cancer Population 40–79 M 180 110 C Questionnaire 0.3 (0.1–0.7) C 0.7 (0.4–1.3) C — C
USA (105) Registry based F 204 119 C Self-report (OPA, LPA) 0.5 (0.3–0.9) C 0.5 (0.3–0.9) C —
Slattery et al., 1997 Different States in Population M 1099 1290 C Questionnaire 0.6 (0.5–0.8) C S C
USA (106) USA based F 894 1120 C Interview (LPA) 0.6 (0.5–0.8) C S
Tang et al., 1999 Taiwan Medical Hospital 33–80 M 92 92 CR Questionnaire 0.3 (0.1–0.8) CR S C
Taiwan (113) Centre based F 71 71 CR Interview (LPA) 0.2 (0.–0.8) C S
0.4 (0.1–1.5) R NS
0.8 (0.3–1.9) CR NS
http://www.acsm-msse.org
FIGURE 2—(A) Relative risk of colon cancer with 95% confidence intervals among persons with high versus low physical activity (LPA and OPA)
in cohort (F) and case-control studies (䡩) (see references). (B) The dose-response relationship between LPA (categories and MET-hours per week)
and colon cancer risk in cohort and case-control studies (see references) including > 100 colon cancer cases. Males (dashed lines): cohort studies
(F) and case-control studies (䡩). Females (solid lines): cohort studies (F) and case-control studies (䡩).
conducted on physical activity for the primary prevention primary prevention. Even a small protective effect of
of cancer. Although many studies suggest an association physical activity on cancer risk may be of considerable
between physical activity and cancer risk (overall and importance for public health as the population ages and a
site-specific), the precise quantitative characteristics of a sedentary lifestyle increases worldwide.
potential threshold effect or the dose-response remains
undefined. Therefore, the aim of the present study was to
METHODS
examine whether there is a dose-response between total
volume of physical activity and indexes of morbidity and Studies were identified through a systematic review of
mortality of overall and site-specific cancer risk and, published literature available on the MEDLINE and
furthermore, to elucidate quantitative characteristics of PubMed literature databases and also by hand searching
the identified dose-response relations of importance in relevant journals through August 2000. The general
PHYSICAL ACTIVITY AND CANCER RISK Medicine & Science in Sports & Exercise姞 S535
TABLE 3. Studies on physical activity and breast cancer risk, dose-response.
S536
Age at Dose-
Total Follow-Up Baseline Cases Physical Activity RR (95% CI) Highest vs Lowest Physical Activity Response Evidence
Cohort Studies Population (N) Time (yr) (N) Assessment LPA OPA Total LPA OPA Total Category
Albanes et al., 1989 National Health and 7407 7–13 25–74 122 Questionnaire 1.0 (0.6–1.6) 0.9 (0.5–1.7) NS NS C
USA (1) Nutrition Survey Interview (LPA, OPA)
Calle et al., 1998 Population Iowa 563,395 9 ⱖ29 1780 Questionnaire 1.1 (1.0–1.3) — C
USA (12) (Fatal) Self-report (OPA)
Cerhan et al., 1998 Population Iowa 1806 20 65–102 46 Questionnaire 0.2 (0.2–0.9) — C
USA (15) 65⫹ Interview (LPA, OPA)
Dorgan et al., 1994 Population 2307 28 ⱖ35 117 Questionnaire 1.6 (0.9–3.0) NS C
USA (24) Interview (LPA, OPA)
Fraser and Shavlik, 1997 Adventists 20,341 6 ⱖ24 218 Questionnaire 0.7 (0.5–0.9) — C
USA (28) Self-report (LPA, OPA,
lifetime)
Frisch et al., 1987 College alumni 5398 1–56 18–22 69 Questionnaire 0.5 (0.3–1.0) — C
USA (31) Self-report
College athletics
Moore et al., 2000 Population sample 37,105 12 55–69 1380 Questionnaire 0.9 (0.8–1.1) — C
USA (83) Iowa driver’s license Self-report (LPA)
Moradi et al., 1999 Population census 1,940,510 18 All ages 51,520 Occupational titles (OPA) 50–59 yr S C
Sweden (85) 0.8 (0.6–0.9)
Paffenbarger et al., 1987 College alumni 4706 28–52 18–22 46 Questionnaire 0.96 (P ⫽ 0.92) NS C
USA (89) Self-report
College athletics (LPA)
Pukkala et al., 1993 Teachers’ college 10,038 24 18–22 228 Self-report 0.7 (0.6–0.8) — C
http://www.acsm-msse.org
TABLE 3. Continued
Physical Activity RR (95% CI) Highest vs Lowest Physical Activity Dose-Response Evidence
Case-Control Studies Study Population Sources of Controls Age Controls (N) Cases (N) Assessment LPA OPA Total LPA OPA Total Category
Coogan et al., 1996 Cancer registries Driver’s license, ⬍75 9453 6835 Occupational titles 1.2 (1.1–1.2) — C
USA (20) Population Medicare (OPA)
Coogan et al., 1997 4 state cancer Driver’s license, ⬍74 6783 4863 Telephone interview (OPA) 0.8 (0.6–1.1) S C
USA (21) registries Medicare
Coogan et al., 1999 General population Population based All 670 233 Telephone Heavy jobs: NS C
USA (22) Interview (OPA) ⬍10 yr 0.7
(0.4–1.3)
ⱖ 10 yr 1.7
(0.9–3.3)
D’Avanzo et al., 1997 General population Hospital based 23–74 2588 2569 Questionnaire 0.7 (0.4–1.1) 0.6 (0.4–1.0) NS S C
Italy (23) Interview (LPA, OPA)
Dosemeci et al., 1993 Hospitals Hospital based All 244 241 Occupation (OPA) 1.4 (0.3–3.5) NS C
Verloop et al., 2000 Population Population based 20–54 918 918 Questionnaire 0.7 (0.6–0.9) S C
Netherlands (126) Interview (LPA, OPA)
S537
RR, relative risk; CI, confidence interval; LPA, leisure time physical activity; OPA, occupational physical activity; S, significant (P ⬎ 0.05); NS, nonsignificant.
FIGURE 3—(A) Relative risk of breast cancer with 95% confidence intervals among persons with high versus low physical activity (LPA and OPA)
in cohort (F) and case-control studies (䡩) (see references). (B) The dose-response relationship between LPA (categories and MET-hours per week)
and breast cancer risk in cohort and case-control studies (see references) including > 100 breast cancer cases. Females— cohort studies (F) and case
control studies (䡩).
inclusion criteria were 1) studies focusing on primary assessments and a great variety in the characteristics of the
prevention of overall and/or site-specific cancer; 2) a populations studied.
quantitative description of the physical activity variable
was described; and 3) the outcome measures including
indexes of morbidity and mortality for overall and/or Physical Activity and Overall Cancer Risk
site-specific cancer. Physical activity has marked effects on many functions of
A dose-response relationship was especially elaborated in the human body, which may influence overall cancer risk
relation to colon and breast cancer in studies including ⬎ (54). These effects include direct mechanical processes such
100 cases, respectively. Multiple results from the same as improved circulation, ventilation and bowel transit time,
study were included only if they contained other character- improved energy balance and immune function, and possi-
istics of the exposure variable (physical activity) or the bly the capacity to perform DNA repair (Fig. 1).
relevant cancer type. Comparisons are made between stud- Among the 17 observational studies identified (Table 1),
ies using a great variety of, sometimes crude, physical all were follow-up studies, most contained information on
S538 Official Journal of the American College of Sports Medicine http://www.acsm-msse.org
TABLE 4. Studies on physical activity and endometrial cancer risk, dose-response.
Follow-Up Age at Baseline Physical Activity RR (95% CI) Highest vs Lowest Physical Activity Dose-Response Evidence
Cohort Studies Study Population Total (N) Time (yr) Cases (N) Assessment LPA OPA Total LPA OPA Total Category
Moradi et al., 1998 Record linkage 1,440,839 19 16–95 12,332 Occupational title (OPA) 0.8 (0.6–1.0) — C
Evidence
Category
Evidence
Category
127), and some contained information on overall cancer
C
incidence (1,19,108). Populations in North America (11
C
studies), Europe (seven studies), and Asia (one study) were
Total
Total
included, and only seven studies included women (Table 1).
Dose-Response
Dose-Response
Taylor and colleagues observed as early as 1962 that sed-
OPA
—
entary workers were at increased risk of developing cancer
OPA
NS
compared with active men, indicating the role of occupa-
LPA
NS
LPA
risk (115). A significant protective effect of leisure time or
Total
Total
RR (95% CI) Highest vs Lowest
RR (95% CI) Highest vs Lowest
workers
OPA
0.3 (0.00–10)
OPA and cancer mortality, or overall cancer incidence, was re-
ported for women compared with men. An estimation of the
effect of leisure time physical activity (LPA) and OPA on
1.7 (0.8–3.2) vs
1.6 (1.1–2.1)
2.1 (1.2–3.4)
No effect
Assessment
Physical Activity
Occupational title
Self-report (LPA)
Questionnaire
language)
595
49
51
Controls (N)
55–69
18–22
30⫹
244
1980–84
All
Time
Hospital based
10,038
tivity may shorten the fecal transit time and thereby reduce
the period of contact between carcinogens and mucosal
Study Population
60,61,66,69,71,72,74 –76,89,91,100,105,106,108,110,113,
Cohort Studies
Mink et al., 1996
China (136)
USA (81)
or both activities combined (Fig. 2A). A significant inverse activity in a cohort study (58) suggest that continuous, rather
crude graded dose-response association between LPA and than short-term activity is of importance.
colon cancer was observed in 21 (6,10,11,18,19,25,39,57, A reduction in bowel transit time because of physical
66,74,76,91,106,113,114,118,119,124,129,130,132) of 33 activity may account for the observed effect on colon cancer
observational studies (Table 2, Table 7, and Fig. 2B). When and the absence of a relationship between physical activity
including studies with at least 100 cases, the dose-response and rectum cancer. In 80% of the 24 studies identified,
associations seems to be especially dependent on moderate- including 12,055 cancer cases localized in the rectum, no
heavy-vigorous physical activity (76) (Fig. 2B). This situa- association between physical activity and rectal cancer was
tion can be illustrated in studies using MET-hours per week observed (Table 2).
(39,76). These observations are demonstrated for both men Breast, endometrial, and ovarian cancer. Endog-
and women, with a somewhat stronger dose-response rela- enous sex hormones (estradiol, progesterone) are strongly
tionship for men compared with women (Fig. 2B), without implicated in the etiology of breast and endometrial cancer
suggesting publication bias (101). Those men and women and possibly also ovarian cancer. Given that physical activ-
who reported that more than 1000 kcal·wk-1 of energy were ity may modulate production, metabolism, and excretion of
expended in vigorous activity through at least three time these hormones, protection against these cancers by means
periods in their lives were observed to have a 40% reduction of physical activity is biologically plausible.
in colon cancer risk (106). Men who were highly active Observations from 26 (7, 13, 15, 21, 23, 28, 31, 43, 53, 65, 77,
(energy expenditure of ⬎2500 kcal·wk-1 at two assess- 80, 82, 85, 86, 94, 97, 102, 112, 120, 122, 124, 126, 134) of 41
ments) had half the risk of developing colon cancer relative studies (1, 7, 12, 13, 15, 17, 20–25, 28, 30, 31, 34, 43, 47, 53, 65,
to inactive men (1000 kcal·wk-1). In another study, 21 73, 77, 80, 82, 83, 85, 86, 89, 94, 96, 97, 99, 102, 108, 112, 120,
MET-hours per week were associated with a 50% reduction 122, 124, 126, 134, 136) including 108,031 breast cancer cases
in colon cancer risk (76) (Fig. 2B), which reflects the fact demonstrate that both OPA and LPA are associated with about a
that approximately 4 h of moderate or 3 h of high-intensity 30% reduction in breast cancer risk in pre-, peri-, and postmeno-
LPA weekly is necessary to reduce colon cancer risk in pausal women, with a graded dose-response relationship reported
middle-aged American women. Some studies suggest a in 16 (7,13,21,23,65,77,80,82,85,86,97,99,102,120,122,126) of 28
greater protective effect on the left than on the right colon studies (Table 3 and Fig. 3B). Findings are less consistent than for
(38), and in lean than in obese persons (119), which is also colon cancer, and the magnitude of the reported associations is
observed to differ by sex (119). generally lower, which may reflect a genuinely weaker relation-
No effect of physical activity related to time period or ship. An alternative explanation is that the strength of the physical
susceptible period of exposure has been observed. However, activity–breast cancer association varies across the lifespan and in
lack of influence of physical activity during adulthood subgroups, as it does for more established risk factors (e.g., repro-
(25,72,89) and an increased effect observed for long-term ductive factors, body mass index). The actual amount of physical
PHYSICAL ACTIVITY AND CANCER RISK Medicine & Science in Sports & Exercise姞 S541
TABLE 6. Studies on physical activity and prostate cancer risk, dose-response.
Age at
S542
RR (95% CI) Highest vs Lowest Physical Activity Dose-Response
Study Total Follow-Up Baseline Cases Physical Activity Evidence
Cohort Studies Population (N) Time (yr) (N) Assessment LPA OPA Total LPA OPA Total Category
Albanes et al., 1989 National Health and 5141 7–13 25–74 122 Questionnaire 0.8 (0.4–1.4) 0.6 (0.3–1.0) NS S C
USA (1) Nutrition Survey Interview (LPA, OPA)
Cerhan et al., 1997 Iowa Rural Health 3673 12 65–101 71 Questionnaire (LPA) 1.9 (1.0–3.5) S C
USA (14) Study
Clemmesen, 1998 Copenhagen male 5248 15 40–59 113 Questionnaire (LPA) 1.3 (0.7–2.3) NS C
Denmark (19) Cohort
Giovannucci et al., Health professionals 47,542 12 40–75 1362 Questionnaire (LPA) 0.9 (0.8–1.1) S C
1998 MET 0.5 (0.2–0.9)
USA (40)
Hartman et al., 1998 Participators 29,133 9 50–69 317 Questionnaire (LPA, OPA) 0.4 (0.2–0.9) S C
Finland (42) (smokers) in a
randomized trial
(alpha-
tocopherol)
Hsing et al., 1994 Shanghai Record 1980–84 All 264 Occupational title (OPA) 0.9 (0.7–1.1) P ⫽ 0.06 C
China (45) Record linkage linkage
1980–84
Lee et al., 1992 Harvard Health 17,719 26 30–79 419 Questionnaire 0.9 (0.6–1.2) NS C
USA (59) Alumni Study Self-report (LPA) 70⫹ yr 0.5 (0.3–1.0) NS
Lee et al., 1994 Harvard alumni 17,607 26 30–79 454 Questionnaire 0.6 (0.2–1.4) NS C
USA (60) Self-administered (LPA)
Liu et al., 2000 Physician Health 22,071 11.1 40–84 982 Questionnaire 1.1 (0.9–1.4) NS C
http://www.acsm-msse.org
TABLE 6. Continued
Evidence
Category
Evidence
Category
studies been reported as leisure time physical activity for at least 4
C
h·wk-1 (7,97,120) of at least moderate intensity (4–5 MET) (126)
Total or continuous vigorous activity (24.5 MET-h·wk-1) (13). A dose-
Total
response relationship was especially observed in case-control stud-
NS
Dose-Response
Dose-Response
ies in where MET-hours per week was assessed (Fig. 3B). LPA
during puberty (73,126) may be particularly important for reduc-
OPA
OPA
NS
S
ing breast cancer risk. However, continuous high levels of LPA
throughout life may be just as important as physical activity in
LPA
—
LPA
—
S
S
puberty (28,73,126).
Of 12 studies (25,41,44,49,64,84,88,94,103,109,116,136)
RR (95% CI) Highest vs Lowest Physical
2.0 (0.6–6.9)
Total
RR (95% CI) Highest vs Lowest Physical
1.0 (0.6–2.0)
1.4 (0.7–2.5)
0.9 (0.6–1.3)
significant (20 – 80%) reduced risk of endometrial cancer
OPA
Activity
Activity
OPA
0.5 (0.3–0.9)
0.7 (0.5–0.9)
2.6 (1.1–5.9)
LPA
Questionnaire (LPA,
Questionnaire (LPA,
Occupational (OPA)
Energy expenditure
Physical Activity
Occupational title
24 h (LPA, OPA)
Assessment
Assessment
Activity in teens
College athletics
Sitting time
OPA)
OPA)
191
794
510
212
45
47
19–50
16,895
794
996
251
Of 28 published studies (1, 2, 11, 14, 19, 25, 40, 42, 45, 48, 56,
Age (yr)
28.62
15–49
15–79
59, 60, 68, 70, 87, 89, 90, 93, 100, 108, 111, 118, 124, 125, 128,
16.3
⬎20
All
All
General practitioners
Finance Property
53,242
Study Population
Cancer Registry
Cancer Registries
England, Wales
White Missouri
Ontario Cancer
Registry
Hospital
Canada (98)
Turkey (25)
USA (11)
USA (90)
16
10
6
Dose-Response
Positive
—
—
1
1
No
14
19
5
Gender differences
Menopausal status
Latency of disease
distal location?
Carcinoma in situ
Characteristics
Disease
Proximal and
Histology?
Histology
Histology
Histology
FIGURE 5—Relative risk of lung cancer with 95% confidence inter-
vals among persons with high versus low physical activity (LPA and
Physical Activity
Duration, Time)
37 studies on OPA
22 studies on OPA
19 studies on OPA
13 studies on OPA
30 studies on LPA
13 studies on LPA
32 studies on LPA
18 studies on LPA
9 studies on OPA
3 studies on OPA
6 studies on OPA
6 studies on OPA
long-term activity
9 studies on LPA
1 studies on LPA
5 studies on LPA
7 studies on LPA
Lung cancer. It is well established that physical activ-
ity improves ventilation and perfusion, which may in turn
reduce both the concentration of carcinogenic agents in the
airways and the duration of agent–airway interaction. How-
ever, the association of physical activity with lung cancer
has only been elaborated in 11 studies (1, 11, 19, 25, 60, 62,
18 case-control
14 case-control
5 case-control
5 case-control
1 case-control
4 case-control
3 case-control
1 case-control
Association Overall (High vs Low)
Negative
89,90,100,108,121) including 7,726 men and women, and
17 cohort
12 cohort
1 cohort
3 cohort
9 cohort
0 cohort
5 cohort
most of these studies were conducted in men only (Table 8).
Findings from 6 (1,11,60,62,100,121) of these 11 studies
35
26
13
6
6
(five cohort studies and one case-control study) support a
Positive
—
0
1
inverse graded dose-response relationship (Fig. 5). No stud-
LPA, leisure time physical activity; OPA, occupational physical activity; BMI, body mass index; MET, metabolic equivalent.
ies suggested an increased risk attributable to physical ac-
tivity. These studies indicate that a continuous 4 h·wk-1 of
No
13
17
15
12
5
hard leisure time activity in order to keep fit (121), and
participation in activities of at least moderate activity
Adjustments Confounding
exogenous hormones
(⬎4 –5 MET), but not light activity (⬍4 –5 MET) (62),
hormone (HRT, OC)
Cryptorchidism, hernia
inguinalis, family
hormones (HRT)
history, BMI
adjustments for smoking and other possible risk factors. An
effect of physical activity related differently to various his-
alcohol
history
Diet, BMI
Cases (N)
12,055
108,031
14,909
792
22,727
2051
7164
15
23
10
18
18
24
41
12
28
11
Endometrial
Colorectal
Testicular
Lung
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