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Biomedical subjects

Paolo Boffetta

Publications and source records attributed to Paolo Boffetta.

At least 127 records · Page 7Linked to original sources
PubMed2003

Mortality and cancer incidence of workers in Finnish road paving companies.

BACKGROUND: This study, a component of the International Agency for Research on Cancer (IARC) Multicentric Study on Cancer Risk Among European Asphalt Workers, aimed at identifying major mortality risks among workers in Finnish road paving companies. METHODS: The Finnish cohort was comprised of 9,643 men and women from six road paving companies. The mortality of men employed during at least one season (5,676) was followed up from 1964 until end of 1994; an average of 17 years. Standardized mortality ratios (SMR) and relative risks (RR), the latter based on multivariate Poisson regression models were estimated by occupational group and by various metrics of occupational exposures. RESULTS: All-cause mortality was elevated (SMR 1.11, 95% confidence interval, CI 1.03-1.20), mainly due to excesses in accidents, poisonings, and violence (1.29; CI 1.12-1.49), and lung cancer (1.38; 1.03-1.81). Workers exposed to bitumen fumes had a slightly elevated mortality from lung cancer (1.16; 0.69-1.83). Multivariate Poisson regression models with 15-year lag period suggested trends by cumulative exposure to coal tar, organic vapors, silica dust, diesel exhaust, and bitumen fume. CONCLUSIONS: The elevated mortality from external causes among Finnish building/ground construction workers was probably due to living conditions and related lifestyles. Some evidence was found for a risk of lung cancer due to occupational exposure, but the confirmation of these findings would require a longer follow-up and improved control for confounding.

Accidental Falls↗
PubMed2003

Performance of different exposure assessment approaches in a study of bitumen fume exposure and lung cancer mortality.

BACKGROUND: We compared performance of different exposure assessment approaches in a cohort study of cancer risk among European asphalt workers. METHODS: Three bitumen fume exposure indices (duration of exposure (years), average exposure (mg/m3) and cumulative exposure (mg/m3*years)) and two latency models (with and without a 15 year lag) were considered for an association between lung cancer mortality and bitumen fume. RESULTS: There was no association between lung cancer risk and either duration or cumulative exposure. However, there was the suggestion of an increase in lung cancer risk accompanying rise in average exposure. Only models with average bitumen fume exposure (with or without lag) improved model fit, albeit to the same extent. CONCLUSIONS: Constructing quantitative indices of exposure intensity was justified because they produced the greatest improvement in fit of models that explored possible relationship between bitumen fume exposure and lung cancer risk. The identified associations require further investigation.

Cohort Studies↗
PubMed2003

Cancer mortality among European asphalt workers: an international epidemiological study. I. Results of the analysis based on job titles.

BACKGROUND: Inhalation of bitumen fumes is potentially carcinogenic to humans. METHODS: We conducted a study of 29,820 male workers exposed to bitumen in road paving, asphalt mixing and roofing, 32,245 ground and building construction workers unexposed to bitumen, and 17,757 workers not classifiable as bitumen workers, from Denmark, Finland, France, Germany, Israel, the Netherlands, Norway, and Sweden, with mortality follow-up during 1953-2000. We calculated standardized mortality ratios (SMRs) and 95% confidence intervals (CIs) based on national mortality rates. Poisson regression analyses compared mortality of bitumen workers to that of building or ground construction workers. RESULTS: The overall mortality was below expectation in the total cohort (SMR 0.92, 95% CI 0.90-0.94) and in each group of workers. The SMR of lung cancer was higher among bitumen workers (1.17, 95% CI 1.04-1.30) than among workers in ground and building construction (SMR 1.01, 95% CI 0.89-1.15). In the internal comparison, the relative risk (RR) of lung cancer mortality among bitumen workers was 1.09 (95% CI 0.89-1.34). The results of cancer of the head and neck were similar to those of lung cancer, based on a smaller number of deaths. There was no suggestion of an association between employment in bitumen jobs and other cancers. CONCLUSIONS: European workers employed in road paving, asphalt mixing and other jobs entailing exposure to bitumen fume might have experienced a small increase in lung cancer mortality risk, compared to workers in ground and building construction. However, exposure assessment was limited and confounding from exposure to carcinogens in other industries, tobacco smoking, and other lifestyle factors cannot be ruled out.

Adult↗
PubMed2003

Cancer mortality among European asphalt workers: an international epidemiological study. II. Exposure to bitumen fume and other agents.

BACKGROUND: An increased risk of lung cancers among asphalt workers has been suggested in epidemiological studies based on large scale statistical analyses. METHODS: In a multi-country study of 29,820 male workers employed in road paving, asphalt mixing and roofing, 32,245 ground and building construction workers and 17,757 other workers from Denmark, Finland, France, Germany, Israel, the Netherlands, Norway, and Sweden, with mortality that was documented from 1953-2000. Exposures to bitumen fume, coal tar, 4-6 ring polycyclic aromatic hydrocarbons, organic vapor, diesel exhaust, asbestos, and silica dust were assessed via a job-exposure matrix. Standardized mortality ratios (SMRs) and 95% confidence intervals (CIs) based on national mortality rates, as well as relative risks (RRs) based on Poisson regression models were calculated. RESULTS: The SMR of lung cancer among workers exposed to bitumen fume (1.08, 95% CI 0.99-1.18) was comparable to that of non-exposed workers (SMR 1.05, 95% CI 0.92-1.19). In a sub-cohort of bitumen-exposed workers without exposure to coal tar, the SMR of lung cancer was 1.23 (95% CI 1.02-1.48). The analysis based on the semi-quantitative, matrix-based exposures in the whole cohort did not suggest an increased lung cancer risk following exposure to bitumen fume. However, in an analysis restricted to road pavers, based on quantitative estimate of bitumen fume exposure, a dose-response was suggested for average level of exposure, applying a 15-year lag, which was marginally reduced after adjustment for co-exposure to coal tar. The results for cancer of the head and neck were similar to those of lung cancer, although they were based on a smaller number of deaths. There was no clear suggestion of an association with bitumen fume for any other neoplasm. CONCLUSIONS: The results of the analysis by bitumen fume exposure do not allow us to conclude on the presence or absence of a causal link between exposure to bitumen fume and risk of cancer of the lung and the head and neck.

Adult↗
PubMed2003

Estimating exposures in the asphalt industry for an international epidemiological cohort study of cancer risk.

BACKGROUND: An exposure matrix (EM) for known and suspected carcinogens was required for a multicenter international cohort study of cancer risk and bitumen among asphalt workers. METHODS: Production characteristics in companies enrolled in the study were ascertained through use of a company questionnaire (CQ). Exposures to coal tar, bitumen fume, organic vapor, polycyclic aromatic hydrocarbons, diesel fume, silica, and asbestos were assessed semi-quantitatively using information from CQs, expert judgment, and statistical models. Exposures of road paving workers to bitumen fume, organic vapor, and benzo(a)pyrene were estimated quantitatively by applying regression models, based on monitoring data, to exposure scenarios identified by the CQs. RESULTS: Exposures estimates were derived for 217 companies enrolled in the cohort, plus the Swedish asphalt paving industry in general. Most companies were engaged in road paving and asphalt mixing, but some also participated in general construction and roofing. Coal tar use was most common in Denmark and The Netherlands, but the practice is now obsolete. Quantitative estimates of exposure to bitumen fume, organic vapor, and benzo(a)pyrene for pavers, and semi-quantitative estimates of exposure to these agents among all subjects were strongly correlated. Semi-quantitative estimates of exposure to bitumen fume and coal tar exposures were only moderately correlated. EM assessed non-monotonic historical decrease in exposures to all agents assessed except silica and diesel exhaust. CONCLUSIONS: We produced a data-driven EM using methodology that can be adapted for other multicenter studies.

Cohort Studies↗
PubMed2003

Serum organochlorine levels and history of lactation in Egypt.

We conducted a study in Egypt to assess the determinants of organochlorine serum levels among premenopausal women and the risk of premenopausal breast cancer for women with high organochlorine serum levels. We included 69 breast cancer patients and 53 controls consisting of visitors to the hospitals of the cancer patients. We found low levels of dichlorodiphenyldichloroethylene (DDE), total dichlorodiphenyltrichloroethane, and beta-hexacholorhexane (beta-HCH) in most subjects. Mean DDE levels were 12.7 +/- 20.3 ppb for cases and 16.6 +/- 30.1 ppb for controls (P = 0.60); beta-HCH levels were 2.1 +/- 3.8 ppb for patients and 2.1 +/- 3.9 ppb for controls (P = 0.71). Interestingly, subjects with low levels had breast fed their children for an average period of 18 months. Women with no lactation history had much higher organochlorine levels than women who breast fed (P = 0.002 for DDE). Younger age, older age at first childbirth, and shorter duration of breast feeding were significant predictors of higher levels of serum DDE levels. Younger age, older age at first childbirth, and higher body mass index were significant predictors of higher beta-HCH levels. This study suggests that organochlorine serum levels in Egyptian women are quite low, but indicates an effect of breast feeding in eliminating organochlorines, which would imply exposure to children. Organochlorine serum level was not a risk factor of breast cancer in this population.

Adult↗
PubMed2003

Occupation and larynx and hypopharynx cancer: a job-exposure matrix approach in an international case-control study in France, Italy, Spain and Switzerland.

OBJECTIVE: To investigate the effect of exposure to occupational agents on the risk of hypopharyngeal/laryngeal cancer. METHODS: Case-control study conducted during 1979-1982 in six centres in South Europe. An occupational history and information on exposure to non-occupational factors were collected for 1010 male cases of hypopharyngeal/ laryngeal cancer as well as for 2176 population controls. The exposure to 10 occupational agents was assessed through a job-exposure matrix. As occupational histories had been collected since 1945 major analyses were restricted to subjects aged less than 55 years (315 cases and 819 controls). RESULTS: Significant elevated risks adjusted for non-occupational variables (smoking, alcohol consumption and diet) and other occupational exposures were consistently found for organic solvents (odds ratio (OR) for ever-exposure: 1.7, 95% confidence interval: 1.1-2.5) and asbestos (OR: 1.6, 1.0-2.5). A significant positive trend for both probability of exposure and duration was found for exposure to solvents. A positive association between exposure to formaldehyde and laryngeal cancer was also suggested. No association was found for exposure to arsenic and compounds, chromium and compounds, and polycyclic aromatic hydrocarbons. Analyses restricted to subjects aged 55 or more did not show elevated risks, with the exception of wood dust (OR: 1.8, 1.3-2.7). CONCLUSIONS: In our study occupational exposure to solvents was associated with an increased risk of hypopharyngeal/laryngeal cancer. Results also provide additional evidence of an excess of risk for exposure to asbestos.

Adult↗
PubMed2003

Occupation and larynx and hypopharynx cancer: an international case-control study in France, Italy, Spain, and Switzerland.

OBJECTIVE: To estimate risks for laryngeal/hypopharyngeal cancer associated with occupational titles and industrial activities. METHODS: A multicentre population-based case-control study was conducted in the early 1980s in six southern European areas. Analyses included 1010 male cases and 2176 controls. Odds ratios (ORs) (adjusted for age, study area, tobacco consumption, and alcohol consumption) were estimated for 156 occupations and 70 industrial activities. RESULTS: An excess risk has been confirmed for categories of construction workers, potters (OR: 5.91, 95% confidence intervals 1.46-24.0), butchers (2.53, 1.22-5.22), barbers (2.33, 1.00-5.40), laborers not otherwise specified (1.52, 1.12-2.06), as well as for men who had been employed in railway transport (1.52, 0.97-2.39), shipbuilding (2.05, 0.89-4.94), and hotels (2.06, 0.89-4.75). An association was also found for shoe finishers (3.23, 0.75-13.9), loggers (2.07, 0.87-4.90), and some groups of metal workers. ORs for loggers, butchers, railway transport workers, laborers, and reinforced concreters increased with duration of employment. The suggestion of a risk for machine operators among woodworkers (3.10, 0.92-10.5) conflicts with previous findings. No significant excess of risk was found for categories previously reported to be associated with laryngeal and hypopharyngeal cancer, such as drivers, mechanics, welders, machinists, and painters. CONCLUSIONS: The present study provides additional evidence to the hypothesis of a risk of cancer of the larynx/ hypopharynx for workers engaged in jobs in the construction, metal, textile, ceramic, and food industries and in railway transport. Loggers were also found at risk; a previously unreported finding.

Adolescent↗
PubMed2003

Cancer incidence among male Swedish veterinarians and other workers of the veterinary industry: a record-linkage study.

OBJECTIVE: To investigate the risk of cancer among veterinarians in a large record-linkage study from Sweden. METHODS: We used the nationwide, Swedish Cancer Environment Registry III, which links the Cancer Register data for 1971-1989 to the national population censuses from 1960 and 1970, to compare the incidence of cancer among male veterinarians to that of the remaining part of the active population using multivariable Poisson regression models and standardized incidence ratios. One thousand one hundred and seventy eight men classified as veterinarians or workers in the veterinary industry at either census were identified. RESULTS: Veterinarians in the veterinary industry experienced increased risk of esophageal (relative risk (RR) 3.78, 95% confidence interval (CI) 1.42-10.09), colon (RR: 2.36, 95% CI: 1.42-3.91), pancreatic (RR: 2.10, 95% CI: 0.94-4.68) and brain (RR: 2.51, 95% CI: 1.04-6.03) cancers as well as melanoma of the skin (RR: 2.77, 95% CI: 1.24-6.17). Similar excess risks were observed when veterinarians were compared with individuals of similar socioeconomic status. CONCLUSION: The increased risks of esophageal, colon, pancreatic and brain cancers as well as melanoma observed among veterinarians did not seem to be explained by the high socio-economic status of this occupational group. Therefore, it is possible that some of these results reflect the carcinogenicity of occupational exposures, including animal viruses, solar or ionizing radiations and anesthetics.

Adult↗
PubMed2003

Occupation and bladder cancer among men in Western Europe.

OBJECTIVES: We examined which occupations and industries are currently at high risk for bladder cancer in men. METHODS: We combined data from 11 case-control studies conducted between 1976-1996 in six European countries. The study comprised 3346 incident cases and 6840 controls, aged 30-79 years. Lifetime occupational and smoking histories were examined using common coding. RESULTS: Odds ratios for eight a priori defined high-risk occupations were low, and with the exception of metal workers and machinists (OR = 1.16, 95% CI = 1.02-1.32), were not statistically significant. Higher risks were observed for specific categories of painters, metal, textile and electrical workers, for miners, transport operators, excavating-machine operators, and also for non-industrial workers such as concierges and janitors. Industries entailing a high risk included salt mining, manufacture of carpets, paints, plastics and industrial chemicals. An increased risk was found for exposure to PAHs (OR for highest exposure tertile = 1.23, 95% CI = 1.07-1.4). The risk attributable to occupation ranged from 4.2 to 7.4%, with an estimated 4.3% for exposure to PAHs. CONCLUSIONS: Metal workers, machinists, transport equipment operators and miners are among the major occupations contributing to occupational bladder cancer in men in Western Europe. In this population one in 10 to one in 20 cancers of the bladder can be attributed to occupation.

Adult↗
PubMed2003

Contribution of environmental factors to cancer risk.

Environmental carcinogens, in a strict sense, include outdoor and indoor air pollutants, as well as soil and drinking water contaminants. An increased risk of mesothelioma has consistently been detected among individuals experiencing residential exposure to asbestos, whereas results for lung cancer are less consistent. At least 14 good-quality studies have investigated lung cancer risk from outdoor air pollution based on measurement of specific agents. Their results tend to show an increased risk in the categories at highest exposure, with relative risks in the range 1.5-2.0, which is not attributable to confounders. Results for other cancers are sparse. A causal association has been established between exposure to environmental tobacco smoke and lung cancer, with a relative risk in the order of 1.2. Radon is another carcinogen present in indoor air which may be responsible for 1% of all lung cancers. In several Asian populations, an increased risk of lung cancer is present in women from indoor pollution from cooking and heating. There is strong evidence of an increased risk of bladder, skin and lung cancers following consumption of water with high arsenic contamination; results for other drinking water contaminants, including chlorination by-products, are inconclusive. A precise quantification of the burden of human cancer attributable to environmental exposure is problematic. However, despite the relatively small relative risks of cancer following exposure to environmental carcinogens, the number of cases that might be caused, assuming a causal relationship, is relatively large, as a result of the high prevalence of exposure.

Air Pollution↗
PubMed2003

CYP1A1 and GSTM1 genetic polymorphisms and lung cancer risk in Caucasian non-smokers: a pooled analysis.

Polymorphisms for genes encoding the metabolic enzymes cytochrome P450 1A1 (CYP1A1) and glutathione S-transferase M1 (GSTM1) might contribute to the variability in individual susceptibility to lung cancer. The role of CYP1A1 and GSTM1 in lung carcinogenesis might be more important at low levels of exposure to carcinogens. Non-smokers represent a population at low exposure, however, they are often overlooked because of the small number of cases. We therefore conducted a pooled analysis of 14 case-control studies on lung cancer in Caucasian non-smokers with comparable information on genetic polymorphisms included in the International Collaborative Study on Genetic Susceptibility to Environmental Carcinogens. We pooled the raw data from a total of 302 cases and 1631 controls with random effects models. We also evaluated the possibility of inclusion bias and conducted influence analyses. The odds ratio (OR) of lung cancer for the variant CYP1A1 Ile(462)Val polymorphism (Ile/Val, Val/Val) was 2.99 [95% confidence interval (95%CI) 1.51-5.91]; this effect was stronger on lung adenocarcinoma (OR 4.85, 95%CI 2.03-11.6). After excluding outlying or imprecise studies, we did not observe a significant effect of the CYP1A1 MspI (T(3801)C) polymorphism or GSTM1 null genotype (OR 1.20, 95%CI 0.89-1.63). Furthermore, our analyses suggested a combined effect of the CYP1A1 Ile(462)Val polymorphism and GSTM1 null genotype. The OR for the combination of the CYP1A1 Ile(462)Val variant and GSTM1 null genotype was 4.67 (95%CI 2.00-10.9) compared with the concurrent presence of the CYP1A1 wild-type and GSTM1 non-null genotype. We did not observe a modification of the effect of the GSTM1 null genotype according to exposure to environmental tobacco smoke and urban/rural residence. Our study therefore suggests that the CYP1A1 Ile(462)Val variant allele might play a role in lung carcinogenesis among non-smokers, possibly in combination with the GSTM1 null genotype.

Case-Control Studies↗
PubMed2003

Assessing exposure misclassification by expert assessment in multicenter occupational studies.

BACKGROUND: In a multicenter case-control study of lung cancer in central and eastern Europe and in Liverpool, exposure to occupational agents was assessed by teams of local experts. We performed an interteam agreement study to estimate the levels of exposure misclassification and the expected attenuation of the risk estimate. METHODS: Eight teams of experts and a reference rater assessed exposure to 70 putative lung carcinogens for 19 jobs. Agreement among teams was calculated through Cohen's kappa, sensitivity, and specificity. RESULTS: Each team showed an overall fair to good agreement with the reference (kappa between 0.53 and 0.64). The agreement among teams in the presence of exposure was excellent for 9 agents, fair to good for 16, and poor for 29. For all agents the specificity was high (average 0.94), although sensitivity varied considerably. CONCLUSIONS: This study of expert exposure assessment showed a small range in reliability among teams of experts, but large differences among agents. This paper presents the range in levels of misclassification that can be expected using experts for assessing occupational exposure to different agents, and the attenuation of the odds ratio that can be expected to result from this misclassification.

Carcinogens, Environmental↗
PubMed2003

Meta-analysis of studies of occupational exposure to vinyl chloride in relation to cancer mortality.

OBJECTIVE: A meta-analysis was made of studies addressing occupational exposure to vinyl chloride in relation to cancer mortality. METHODS: Two recently updated multicenter cohort studies and six smaller studies were identified. For selected neoplasms, standardized mortality ratios (SMR) and 95% confidence intervals (95% CI) were abstracted (or calculated from raw data). In cases of lack of heterogeneity (P-value > or = 0.01), meta-analyses were conducted using a random-effects model. RESULTS: With SMR values ranging from 1.63 to 57.1, all six studies for which these ratios could be obtained suggested an increased risk of liver cancer. For four of these studies, excesses persisted when known cases of angiosarcoma of the liver (ASL) were excluded. The meta-SMR for liver cancers other than ASL (based on the 2 large cohorts) was 1.35 (95% CI 1.04-1.77). The meta-SMR for lung cancer was 0.90 (95% CI 0.77-1.00, based on 5 studies), although higher SMR values were reported in early studies. The meta-SMR for brain cancer, based on 5 studies, was 1.26 (95% CI 0.98-1.62). For soft tissue sarcomas, the meta-SMR based on 4 studies was 2.52 (95% CI 1.56-4.07). The meta-SMR for lymphatic and hematopoietic neoplasms in the 2 large studies was 0.90 (95% CI 0.75-1.01), although 3 of the smaller studies reported significant excesses. CONCLUSIONS: Apart from the known risk of ASL, workers exposed to vinyl chloride may experience an increased risk of hepatocellular carcinoma and soft-tissue sarcoma; however, these results may have been influenced by the underdiagnosis of true ASL. Increased mortality from lung and brain cancers and from lymphatic and hematopoietic neoplasms cannot be excluded; mortality from other neoplasms does not appear to be increased.

Humans↗
PubMed2003

Maté consumption and the risk of squamous cell esophageal cancer in uruguay.

A retrospective hospital-based case-control study was carried out at the Oncology Institute of Montevideo, Uruguay, to investigate the role of maté consumption in esophageal cancer risk. The study included 344 cases with squamous cell carcinoma of the esophagus and 469 controls recruited between January 1988 and August 2000. Maté consumption was significantly associated with an increased risk of developing esophageal cancer and showed a clear dose response, with a relative risk of 2.84 [95% confidence interval (CI), 1.41-5.73] for those drinking more than 1 liter/day of maté as compared with nondrinkers. Subjects who self-reported drinking maté at a very hot temperature had an almost 2-fold increase in risk [odds ratio (OR), 1.87; 95% CI, 1.17-3.00] compared with those drinking warm to hot maté, after adjusting for cumulative consumption of maté. Maté amount and temperature were observed to have independent effects and, although no departure from multiplicativity was observed between the two covariates, those drinking more than 1 liter/day of maté at a very hot temperature had a 3-fold increase in risk (OR, 2.95; 95% CI, 1.30-6.74) compared with those drinking less than 0.5 liter/day of maté at a warm to hot temperature. Subjects with high cumulative exposure to maté in the presence of low alcohol and tobacco exposures presented a lower-risk estimate (OR, 1.52; 95% CI, 0.88-2.62), whereas those with high cumulative exposures to maté, alcohol, and tobacco presented a 7-fold increase in esophageal cancer risk (OR, 7.10; 95% CI, 3.75-13.46). The population-attributable fraction as a result of maté consumption was calculated to be 53%, of which the sole effect of amount and temperature was 14.8 and 12.6% respectively, and 14.9% was attributable to high maté consumption at high temperature.

Adult↗
PubMed2003

Polymorphisms of the DNA repair genes XRCC1, XRCC3, XPD, interaction with environmental exposures, and bladder cancer risk in a case-control study in northern Italy.

Tobacco smoking and occupational exposures are the main known risk factors for bladder cancer, causing direct and indirect damage to DNA. Repair of DNA damage is under genetic control, and DNA repair genes may play a key role in maintaining genome integrity and preventing cancer development. Polymorphisms in DNA repair genes resulting in variation of DNA repair efficiency may therefore be associated with bladder cancer risk. A hospital-based case-control study was conducted in Brescia, Italy, to assess the relationship between polymorphisms in DNA repair genes XRCC1 (Arg(399)Gln), XRCC3 (Thr(241)Met), and XPD (Lys(751)Gln) and bladder cancer risk. A total of 201 male incident bladder cancer cases and 214 male controls with urological nonneoplastic diseases were recruited and frequency-matched on age, period, and hospital of recruitment. Detailed information was collected using a semistructured questionnaire on demographic, dietary, environmental, and occupational factors. Genotypes were determined by PCR-RFLP analysis. The XRCC3 codon 241 variant genotype exhibited a protective effect against bladder cancer [odds ratio (OR), 0.63; 95% confidence interval (CI), 0.42-0.93], which was prominent among heavy smokers (OR, 0.49; 95% CI, 0.28-0.88) but not among never and light smokers. No overall impact of the XRCC1 codon 399 polymorphism was found (OR, 0.86; 95% CI, 0.59-1.28), but a protective influence of the homozygous variant was suggested among heavy smokers (OR, 0.38; 95% CI, 0.14-1.02). XPD polymorphisms did not show an association with bladder cancer (OR, 0.92; 95% CI, 0.62-1.37). There was no statistical evidence of an interaction between these three genetic polymorphisms and either tobacco smoking or occupational exposure to polycyclic aromatic hydrocarbons and aromatic amines. The XRCC3 codon 241 polymorphism had an overall protective effect against bladder cancer that was most apparent among heavy smokers. Similarly, the XRCC1 codon 399 polymorphism also had a protective effect on bladder cancer among heavy smokers. The XPD polymorphism was not, however, associated with bladder cancer risk.

Adult↗
PubMed2003

Meta- and pooled analyses of GSTM1, GSTT1, GSTP1, and CYP1A1 genotypes and risk of head and neck cancer.

Sequence variation in the GSTM1, GSTT1, GSTP1, and CYP1A1 genes may potentially alter susceptibility to head and neck cancers, although evidence from previous studies has not been consistent. To explore these associations, we conducted a meta-analysis of 31 published case-control studies (4635 cases and 5770 controls) and a pooled analysis of original data from nine published and two unpublished case-control studies (2334 cases and 2766 controls). In the meta-analysis, the summary odds ratios (ORs) for head and neck cancer were 1.23 [95% confidence interval (95% CI), 1.06-1.42] for the GSTM1 null genotype, 1.17 (95% CI, 0.98-1.40) for the GSTT1 null genotype, 1.10 (95% CI, 0.92-1.31) for carrying the GSTP1 Val105 allele, and 1.35 (95% CI, 0.95-1.82) for carrying the CYP1A1 Val462 allele. The pooled analysis ORs were 1.32 (95% CI, 1.07-1.62) for the GSTM1 null genotype, 1.25 (95% CI, 1.00-1.57) for the GSTT1 null genotype, 1.15 (95% CI, 0.86-1.53) for carrying the GSTP1 Val105 allele, and 0.98 (95% CI, 0.75-1.29) for carrying the CYP1A1 Val462 allele. Increasing risk of head and neck cancer was observed with inheritance of increasing numbers of modest risk genotypes at the three GST loci (P for trend = 0.04), with the combination of carrying the GSTM1 null, GSTT1 null, and GSTP1 Val105 alleles conferring an OR of 2.06 (95% CI, 1.11-3.81). In conclusion, both the meta- and pooled analysis support modest associations of GSTM1 and GSTT1 genotypes with head and neck cancer risk, and our pooled analysis supports the notion of greater risk when genotypes at multiple GST loci are considered in a multigenic model.

Alleles↗