Biomedical subjects

Mustafa Dosemeci

Publications and source records attributed to Mustafa Dosemeci.

At least 19 recordsLinked to original sources

PubMed2007

Occupational exposure to organochlorine insecticides and cancer incidence in the Agricultural Health Study.

Organochlorine (OC) insecticides have been regulated as possible human carcinogens primarily on the basis of animal studies. However, the epidemiologic evidence is inconsistent. We investigated the relationship between cancer incidence and OC insecticide use among pesticide applicators enrolled in the Agricultural Health Study, a prospective cohort study of 57,311 licensed applicators in Iowa and North Carolina enrolled between 1993 and 1997. Information on ever use of 7 OC insecticides (aldrin, chlordane, DDT, dieldrin, heptachlor, lindane, toxaphene) was collected from a self-administered questionnaire at enrollment. Lifetime exposure-days to OC insecticides were calculated using additional data from a take-home questionnaire completed by 25,291 participants (44% of total). We found no clear evidence of an association between use of OC insecticides and incident cancers (N = 1,150) ascertained through December, 2002. When we focused on individual insecticides and structurally similar groups (aldrin and dieldrin; chlordane and heptachlor), significantly increased relative risks of some cancers were observed for use of some chemicals (rectal cancer and chlordane, lung cancer and dieldrin, non-Hodgkin lymphoma (NHL) and lindane, melanoma and toxaphene, leukemia and chlordane/heptachlor). Some significant decreased relative risks were also observed (colon cancer and aldrin; overall cancer and heptachlor). In conclusion, we did not observe any clear relationship between cancer risk and the use of OC insecticides. Our chemical-specific findings are based on small numbers and multiple comparisons, and should be interpreted with caution; however, some observed associations (lindane and NHL, chlordane/heptachlor and leukemia) are supported by previous evidence.

Adult↗

PubMed2007

Genetic variation in the base excision repair pathway and bladder cancer risk.

Genetic polymorphisms in DNA repair genes may impact individual variation in DNA repair capacity and alter cancer risk. In order to examine the association of common genetic variation in the base-excision repair (BER) pathway with bladder cancer risk, we analyzed 43 single nucleotide polymorphisms (SNPs) in 12 BER genes (OGG1, MUTYH, APEX1, PARP1, PARP3, PARP4, XRCC1, POLB, POLD1, PCNA, LIG1, and LIG3). Using genotype data from 1,150 cases of urinary bladder transitional cell carcinomas and 1,149 controls from the Spanish Bladder Cancer Study we estimated odds ratios (ORs) and 95% confidence intervals (CIs) adjusting for age, gender, region and smoking status. SNPs in three genes showed significant associations with bladder cancer risk: the 8-oxoG DNA glycosylase gene (OGG1), the Poly (ADP-ribose) polymerase family member 1 (PARP1) and the major gap filling polymerase-beta (POLB). Subjects who were heterozygous or homozygous variant for an OGG1 SNP in the promoter region (rs125701) had significantly decreased bladder cancer risk compared to common homozygous: OR (95%CI) 0.78 (0.63-0.96). Heterozygous or homozygous individuals for the functional SNP PARP1 rs1136410 (V762A) or for the intronic SNP POLB rs3136717 were at increased risk compared to those homozygous for the common alleles: 1.24 (1.02-1.51) and 1.30 (1.04-1.62), respectively. In summary, data from this large case-control study suggested bladder cancer risk associations with selected BER SNPs, which need to be confirmed in other study populations.

Adult↗

PubMed2006

Bladder cancer and exposure to water disinfection by-products through ingestion, bathing, showering, and swimming in pools.

Bladder cancer has been associated with exposure to chlorination by-products in drinking water, and experimental evidence suggests that exposure also occurs through inhalation and dermal absorption. The authors examined whether bladder cancer risk was associated with exposure to trihalomethanes (THMs) through ingestion of water and through inhalation and dermal absorption during showering, bathing, and swimming in pools. Lifetime personal information on water consumption and water-related habits was collected for 1,219 cases and 1,271 controls in a 1998-2001 case-control study in Spain and was linked with THM levels in geographic study areas. Long-term THM exposure was associated with a twofold bladder cancer risk, with an odds ratio of 2.10 (95% confidence interval: 1.09, 4.02) for average household THM levels of >49 versus < or =8 micro g/liter. Compared with subjects not drinking chlorinated water, subjects with THM exposure of >35 micro g/day through ingestion had an odds ratio of 1.35 (95% confidence interval: 0.92, 1.99). The odds ratio for duration of shower or bath weighted by residential THM level was 1.83 (95% confidence interval: 1.17, 2.87) for the highest compared with the lowest quartile. Swimming in pools was associated with an odds ratio of 1.57 (95% confidence interval: 1.18, 2.09). Bladder cancer risk was associated with long-term exposure to THMs in chlorinated water at levels regularly occurring in industrialized countries.

Adult↗

PubMed2006

Brain cancer mortality and potential occupational exposure to lead: findings from the National Longitudinal Mortality Study, 1979-1989.

We evaluated the association between potential occupational lead exposure and the risk of brain cancer mortality in the National Longitudinal Mortality Study (NLMS), which is a prospective census-based cohort study of mortality among the noninstitutionalized United States population (1979-1989). The present study was limited to individuals for whom occupation and industry were available (n = 317,968). Estimates of probability and intensity of lead exposure were assigned using a job-exposure matrix (JEM). Risk estimates for the impact of lead on brain cancer mortality were computed using standardized mortality ratio (SMR) and proportional hazards and Poisson regression techniques, adjusting for the effects of age, gender and several other covariates. Brain cancer mortality rates were greater among individuals in jobs potentially involving lead exposure as compared to those unexposed (age- and gender-adjusted hazard ratio (HR) = 1.5; 95% confidence interval (CI) = 0.9-2.3) with indications of an exposure-response trend (probability: low HR = 0.7 (95% CI = 0.2-2.2), medium HR = 1.4 (95% CI = 0.8-2.5), high HR = 2.2 (95% CI = 1.2-4.0); intensity: low HR = 1.2 (95% CI = 0.7-2.1), medium/high HR = 1.9 (95% CI = 1.0-3.4)). Brain cancer risk was greatest among individuals with the highest levels of probability and intensity (HR = 2.3; 95% CI = 1.3-4.2). These findings provide further support for an association between occupational lead exposure and brain cancer mortality, but need to be interpreted cautiously due to the consideration of brain cancer as one disease entity and the absence of biological measures of lead exposure.

Adult↗

PubMed2006

Cancer incidence among pesticide applicators exposed to metolachlor in the Agricultural Health Study.

Metolachlor is one of the most widely used herbicides in the United States. We evaluated the incidence of cancer among pesticide applicators exposed to metolachlor in the Agricultural Health Study, a prospective cohort study of licensed pesticide applicators in Iowa and North Carolina. A total of 50,193 pesticide applicators were included. Detailed information on pesticide exposure and lifestyle factors was obtained from self-administered enrollment questionnaires completed between 1993 and 1997; average length of follow-up was 7.33 years. Two metolachlor exposure metrics were used : (i) lifetime days personally mixed or applied metolachlor and (ii) intensity-weighted lifetime days (lifetime days x an intensity level). Poisson regression analysis was used to estimate relative risks (RR) and 95% confidence intervals (95%CI) for cancer subtypes by tertiles of metolachlor exposure. No clear risk for any cancer subtype was found for exposure to metolachlor. A significantly decreased RR was found for prostate cancer in the highest category of lifetime days exposure (RR = 0.59; 95%CI, 0.39-0.89) and in the second highest category of intensity-weighted lifetime days exposure (RR = 0.66; 95%CI, 0.45-0.97); however, the test for trend was not significant for either exposure metric. A nonsignificantly increased risk was found for lung cancer with lifetime days exposure in the highest category (RR = 2.37; 95%CI, 0.97-5.82, p-trend = 0.03) but not with intensity-weighted lifetime days. Given the widespread use of metolachlor and the frequent detection of metolachlor in both surface and ground water, future analyses of the AHS will allow further examination of long-term health effects, including lung cancer and the less common cancers.

Acetamides↗

PubMed2006

Hair dye use is not associated with risk for bladder cancer: evidence from a case-control study in Spain.

An increased bladder cancer risk has been suggested among users of hair dyes. We evaluated this association among females in a hospital-based case-control study in Spain (152 female incident cases, 166 female controls). The effect of hair dye use was also evaluated among potentially susceptible subgroups defined by NAT1, NAT2, CYP1A2, GSTM1, GSTT1 and GSTP1 genotypes. Use of any hair dye (OR=0.8, CI 0.5-1.4) or of permanent hair dyes (OR=0.8, CI 0.5-1.5) was not associated with increased risk. Small non-significant increases in risks were observed in a lagged analysis that ignores exposures within ten years of diagnosis (OR=1.3, CI 0.8-2.2). No trend in risk with increasing exposure was seen for duration of use, average use or cumulative use. None of the polymorphisms examined significantly modified the hair dye associated risk. Overall, this study does not support an association between hair dye use and bladder cancer.

Aged↗

PubMed2006

Risk of lung cancer from exposure to dusts and fibers in Leningrad Province, Russia.

BACKGROUND: Exposures to several dusts and fibers (DFs) have been established or suggested as etiologic factors for lung cancer. METHODS: To investigate lung cancer risk in relation to exposure to DFs, we identified 540 pathologically-diagnosed lung cancer cases and 582 controls from the 1993-1998 autopsy records of the 88 hospitals of Leningrad Province, Russia. Lifetime job-specific exposure measurements were available for 15 organic, 15 man-made and 28 natural-inorganic agents. RESULTS: In male workers, increased risks were found for linen dust (OR = 3.68, 95% CI 1.00-13.6, adjusted for age, smoking and residence), and unspecified DFs (OR = 1.44, 95% CI 1.07-1.94). Small non-significant excess risks were observed for quartz dust (OR = 1.27; 95% CI 0.83-1.93) and man-made vitreous fibers (MMVFs) (OR = 1.82, 95% CI 0.88-3.75). In female subjects, risks were non-significantly associated with paper dust (OR = 1.77, 95% CI 0.74-4.20), and unspecified DFs (OR = 1.52, 95% CI 0.77-3.03). CONCLUSIONS: The study showed increased lung cancer risk for selected categories of DFs.

Adult↗

PubMed2006

Inter-rater agreement of assessed prenatal maternal occupational exposures to lead.

BACKGROUND: Industrial hygienists' assessments of prenatal occupational exposures based on parental job histories is a promising approach for population-based case-control studies of birth defects and other perinatal outcomes. However, evaluations of inter-rater agreement of such assessments have been limited. METHODS: We examined inter-rater agreement of occupational lead exposure assessments of maternal job reports by industrial hygienists in a population-based case-control study of parental occupational lead exposure and low birth weight. A total of 178 jobs with potential exposure to lead during the 6 months before pregnancy to the end of pregnancy were examined. Three industrial hygienists evaluated these jobs independently for exposure to lead including probability of exposure, type of exposure, route of entry, exposure frequency, duration, and intensity. Inter-rater agreement of these assessments beyond chance was evaluated using the kappa statistic (kappa). RESULTS: In general, inter-rater agreement was greater for assessment of direct exposures than assessment of indirect exposures. However, inter-rater agreement varied with the lead exposure metric under consideration, being: 1) fair to good for type of direct exposure (i.e., inorganic or organic), respiratory exposure and frequency of exposure to direct inorganic lead, hours per day of direct (i.e., inorganic or organic), and intensity of direct inorganic exposure; 2) poor for probability and type of indirect exposure (inorganic or organic); and 3) indeterminate for frequency of direct organic exposure, frequency of indirect exposures (organic or inorganic), and intensity of direct exposures (organic or inorganic). CONCLUSION: Retrospective assessment of maternal prenatal exposures to lead by industrial hygienists can provide some reliable metrics of exposure for studies of perinatal outcomes. Reliability studies of such exposure assessments may be useful for: quantifying the reliability of derived exposure metrics; identifying exposure metrics for exposure-outcome analyses; and determining the reliability of prenatal occupational exposures to other agents of interest.

Adult↗

PubMed2006

Pendimethalin exposure and cancer incidence among pesticide applicators.

BACKGROUND: Pendimethalin, a widely used herbicide, has been classified as a group C possible human carcinogen by the U.S. Environmental Protection Agency. We evaluated the incidence of cancer in relation to reported pendimethelin use among pesticide applicators in the Agricultural Health Study, a prospective cohort of licensed pesticide applicators in Iowa and North Carolina. METHODS: Information on pesticide use came from two questionnaires (enrollment and take-home). The present analysis includes 9089 pendimethalin-exposed and 15,285 nonpendimethalin-exposed pesticide applicators with complete information on pendimethalin use and covariates from a take-home questionnaire. We conducted Poisson regression analyses to evaluate the association of pendimethalin exposure with cancer incidence (mean follow-up = 7.5 years) using two exposure metrics: tertiles of lifetime days of exposure and tertiles of intensity-weighted lifetime days of exposure. RESULTS: Overall cancer incidence did not increase with increasing lifetime pendimethalin use, and there was no clear evidence of an association between pendimethalin use and risks for specific cancers. The risk for rectal cancer rose with increasing lifetime pendimethalin exposure when using nonexposed as the reference (rate ratio = 4.3; 95% confidence interval = 1.5-12.7 for the highest exposed subjects; P for trend = 0.007), but the association was attenuated when using the low exposed as the referent group (P for trend = 0.08). Similar patterns for rectal cancer were observed when using intensity-weighted exposure-days. The number of rectal cancer cases among the pendimethalin-exposed was small (n = 19). There was some evidence for an elevated risk for lung cancer, but the excess occurred only in the highest exposure category for lifetime pendimethalin exposure. The trends for lung cancer risk were inconsistent for different exposure metrics. CONCLUSIONS: We did not find a clear association of lifetime pendimethalin exposure either with overall cancer incidence or with specific cancer sites.

Adult↗

PubMed2006

Risk of lung cancer and exposure to industrial acids, solvents, and metals in leningrad province, Russia.

OBJECTIVE: We sought to investigate the association of occupational exposure to industrial acids, solvents, and metals with lung cancer in Leningrad Province, Russia, where an excess of occupationally related lung cancer was reported recently. METHODS: We identified 540 pathologically diagnosed lung cancer cases and 582 controls from the 1993-1998 autopsy records of the 88 Leningrad Province hospitals. Lifetime job-specific exposure measurements were available for 12 industrial acids, 15 solvents, and 17 metals. RESULTS: Exposures were frequent in the study group and mostly occurred after World War II. However, lung cancer risks for industrial acids (odds ratio [OR] = 1.2; 95% confidence interval [CI] = 0.8-1.7), solvents (OR = 0.8; 95% CI = 0.6-1.2), and metals (OR = 0.8; 95% CI = 0.5-1.0) were not increased. Also, no significant excess risk was found for any of the specific agents investigated. CONCLUSIONS: The excess of occupationally related lung cancer in the Province is not explained by exposure to the agents investigated.

Acids↗

PubMed2006

Occupational and leisure-time physical activity and risk of colon cancer by subsite.

OBJECTIVE: Studies of physical activity and colon cancer risk by anatomic site have provided inconsistent results. METHODS: We analyzed data from a population-based case-control study conducted in Iowa involving 685 colon cancer cases and 2434 control subjects. RESULTS: Among those who reported recreational activity more than twice per week, a 30% risk reduction of colon cancer was observed for all sites with a 40% risk reduction for cancer of the right colon. Occupational physical activity was also associated with a reduced risk of colon cancer. The risk was the lowest for those with both high occupational and recreational physical activity (odds ratio, 0.5; 95% confidence interval, 0.3-0.8). CONCLUSIONS: Increased physical activity was inversely associated with colon cancer risk. The inverse associations were stronger for the right than for the left colon.

Adult↗

PubMed2006

Genetic variation in the nucleotide excision repair pathway and bladder cancer risk.

Nucleotide excision repair (NER) is critical for protecting against damage from carcinogens in tobacco smoke. We evaluated the influence of common genetic variation in the NER pathway on bladder cancer risk by analyzing 22 single nucleotide polymorphisms (SNP) in seven NER genes (XPC, RAD23B, ERCC1, ERCC2, ERCC4, ERCC5, and ERCC6). Our study population included 1,150 patients with transitional cell carcinoma of the urinary bladder and 1,149 control subjects from Spain. Odds ratios (OR) and 95% confidence intervals (95% CI) were adjusted for age, gender, region, and smoking status. Subjects with the variant genotypes for SNPs in four of the seven genes evaluated had small increases in bladder cancer risk compared to subjects with the homozygous wild-type genotypes: RAD23B IVS5-15A>G (OR, 1.3; 95% CI, 1.1-1.5; P = 0.01), ERCC2 R156R (OR, 1.3; 95% CI, 1.1-1.6; P = 0.006), ERCC1 IVS5+33A>C (OR, 1.2; 95% CI, 1.0-1.5; P = 0.06; P(trend) = 0.04), and ERCC5 M254V (OR, 1.4; 95% CI, 1.0-2.0; P = 0.04). A global test for pathway effects indicated that genetic variation in NER characterized by the 22 SNPs analyzed in this study significantly predicts bladder cancer risk (P = 0.04). Pairwise comparisons suggested that carrying variants in two genes could result in substantial increases in risk. Classification tree analyses suggested the presence of subgroups of individuals defined by smoking and NER genotypes that could have substantial increases in risk. In conclusion, these findings provide support for the influence of genetic variation in NER on bladder cancer risk. A detailed characterization of genetic variation in key NER genes is warranted and might ultimately help identify multiple susceptibility variants that could be responsible for substantial joint increases in risk.

Adult↗

PubMed2006

Smoking and bladder cancer in Spain: effects of tobacco type, timing, environmental tobacco smoke, and gender.

We examined the effects of dose, type of tobacco, cessation, inhalation, and environmental tobacco smoke exposure on bladder cancer risk among 1,219 patients with newly diagnosed bladder cancer and 1,271 controls recruited from 18 hospitals in Spain. We used unconditional logistic regression to estimate odds ratios (OR) and 95% confidence intervals (95% CI) for the association between bladder cancer risk and various characteristics of cigarette smoking. Current smokers (men: OR, 7.4; 95% CI, 5.3-10.4; women: OR, 5.1; 95% CI, 1.6-16.4) and former smokers (men: OR, 3.8; 95% CI, 2.8-5.3; women: OR, 1.8; 95% CI, 0.5-7.2) had significantly increased risks of bladder cancer compared with nonsmokers. We observed a significant positive trend in risk with increasing duration and amount smoked. After adjustment for duration, risk was only 40% higher in smokers of black tobacco than that in smokers of blond tobacco (OR, 1.4; 95% CI, 0.98-2.0). Compared with risk in current smokers, a significant inverse trend in risk with increasing time since quitting smoking blond tobacco was observed (> or =20 years cessation: OR, 0.2; 95% CI, 0.1-0.9). No trend in risk with cessation of smoking black tobacco was apparent. Compared with men who inhaled into the mouth, risk increased for men who inhaled into the throat (OR, 1.7; 95% CI, 1.1-2.6) and chest (OR, 1.5; 95% CI, 1.1-2.1). Cumulative occupational exposure to environmental tobacco smoke seemed to confer increased risk among female nonsmokers but not among male nonsmokers. After eliminating the effect of cigarette smoking on bladder cancer risk in our study population, the male-to-female incidence ratio decreased from 8.2 to 1.7, suggesting that nearly the entire male excess of bladder cancer observed in Spain is explained by cigarette smoking rather than occupational/environmental exposures to other bladder carcinogens.

Adult↗

PubMed2006

Use of analgesics and nonsteroidal anti-inflammatory drugs, genetic predisposition, and bladder cancer risk in Spain.

BACKGROUND: We assessed use of nonaspirin nonsteroidal anti-inflammatory drugs (NSAID), aspirin, paracetamol (acetaminophen), phenacetin, and metamizol (dipyrone) and risk of bladder cancer and their interaction with polymorphisms in drug-metabolizing genes. METHODS: We analyzed personal interview data from 958 incident bladder cancer cases and 1,029 hospital controls from a multicenter case-control study in Spain. A drug matrix was developed to estimate cumulative lifetime dose of active ingredients. Polymorphisms in GSTP1, SULT1A1, CYP2E1, CYP2C9, and NAT2 were examined. RESULTS: A significant reduction in bladder cancer risk [adjusted odds ratio (OR), 0.4; 95% confidence interval (95% CI), 0.2-0.9] was observed for regular users of nonaspirin NSAIDs compared with never users. Regular users of aspirin experienced no reduction in risk (OR, 1.0; 95% CI, 0.7-1.5). Regular users of paracetamol had no overall increased risk of bladder cancer (OR, 0.8; 95% CI, 0.4-1.3), but our data suggested a qualitative interaction with the GSTP1 I105V genotype. Subjects with at least one copy of the 359L or 144C variant alleles in the NSAID-metabolizing gene CYP2C9 had a slightly decreased risk of bladder cancer (OR, 0.8; 95% CI, 0.7-1.0; P = 0.037); however, having at least one copy of the 359L or 144C variant alleles did not significantly modify the protective effect of nonaspirin NSAID use. CONCLUSION: Regular use of nonaspirin NSAIDs was associated with a reduced risk of bladder cancer, which was not modified by polymorphisms in the NSAID-metabolizing gene CYP2C9. We found no evidence of an overall effect for paracetamol or aspirin use.

Adult↗

PubMed2006

Cancer incidence among pesticide applicators exposed to cyanazine in the agricultural health study.

BACKGROUND: Cyanazine is a common pesticide used frequently in the United States during the 1980s and 1990s. Animal and human studies have suggested that triazines may be carcinogenic, but results have been mixed. We evaluated cancer incidence in cyanazine-exposed pesticide applicators among the 57,311 licensed pesticide applicators in the Agricultural Health Study (AHS). METHODS: We obtained detailed pesticide exposure information from a self-administered questionnaire completed at enrollment (1993-1997). Cancer incidence was followed through January 2002. Over half of cyanazine-exposed applicators had >or=6 years of exposure at enrollment, and approximately 85% had begun using cyanazine before the 1990s. We used adjusted Poisson regression to calculate rate ratios (RRs) and 95% confidence intervals (CIs) of multiple cancer sites among cyanazine-exposed applicators. We calculated ptrend values, and all statistical tests were two-sided. Two exposure metrics were used: tertiles of lifetime days of exposure (LD) and intensity-weighted LD. RESULTS: A total of 20,824 cancer-free AHS applicators reported ever using cyanazine at enrollment. Cancer incidence comparisons between applicators with the lowest cyanazine exposure and those with the highest exposure yielded the following for the LD metric: all cancers, RR=0.99 (95% CI, 0.80-1.24); prostate cancer, RR=1.23 (95% CI, 0.87-1.70); all lymphohematopoietic cancers, RR=0.92 (95% CI, 0.50-1.72); non-Hodgkin lymphoma, RR=1.25 (95% CI, 0.47-3.35); lung cancer, RR=0.52 (95% CI, 0.22-1.25). CONCLUSIONS: We did not find any clear, consistent associations between cyanazine exposure and any cancer analyzed. The number of sites was small for certain cancers, limiting any conclusion with regard to ovarian, breast, and some other cancers.

Adult↗

PubMed2006

Cancer incidence among pesticide applicators exposed to dicamba in the agricultural health study.

BACKGROUND: Dicamba is an herbicide commonly applied to crops in the United States and abroad. We evaluated cancer incidence among pesticide applicators exposed to dicamba in the Agricultural Health Study, a prospective cohort of licensed pesticide applicators in North Carolina and Iowa. METHODS: Detailed pesticide exposure information was obtained through a self-administered questionnaire completed from 1993 to 1997. Cancer incidence was followed through 31 December 2002 by linkage to state cancer registries. We used Poisson regression to estimate rate ratios and 95% confidence intervals for cancer subtypes by tertiles of dicamba exposure. Two dicamba exposure metrics were used: lifetime exposure days and intensity-weighted lifetime exposure days (lifetime days x intensity score). RESULTS: A total of 41,969 applicators were included in the analysis, and 22,036 (52.5%) reported ever using dicamba. Exposure was not associated with overall cancer incidence nor were there strong associations with any specific type of cancer. When the reference group comprised low-exposed applicators, we observed a positive trend in risk between lifetime exposure days and lung cancer (p = 0.02), but none of the individual point estimates was significantly elevated. We also observed significant trends of increasing risk for colon cancer for both lifetime exposure days and intensity-weighted lifetime days, although these results are largely due to elevated risk at the highest exposure level. There was no apparent risk for non-Hodgkin lymphoma. CONCLUSIONS: Although associations between exposure and lung and colon cancer were observed, we did not find clear evidence for an association between dicamba exposure and cancer risk.

Adult↗

PubMed2006

Occupational exposure to ionizing radiation and electromagnetic fields in relation to the risk of thyroid cancer in Sweden.

OBJECTIVES: This study sought to ascertain the risk of thyroid cancer in relation to occupational exposure to ionizing radiation and extremely low-frequency magnetic fields (ELFMF) in a cohort representative of Sweden's gainfully employed population. METHODS: A historical cohort of 2 992 166 gainfully employed Swedish male and female workers was followed up from 1971 through 1989. Exposure to ELFMF and ionizing radiation was assessed using three job exposure matrices based on industrial branch or occupational codes. Relative risks (RR) for male and female workers, adjusted for age and geographic area, were computed using log-linear Poisson models. RESULTS: Occupational ELFMF exposure showed no effect on the risk of thyroid cancer in the study. However, female workers exposed to high intensities of ionizing radiation registered a marked excess risk (RR 1.85, 95% confidence interval (95% CI) 1.02-3.35]. This trend was not in evidence among the men. CONCLUSIONS: While the study confirms the etiologic role of ionizing radiation, with a higher incidence of thyroid cancer being recorded for the most-exposed female workers, our results do not support the possibility of occupational exposure to ELFMF being a risk factor for the development of thyroid cancer.

Adult↗

PubMed2005

Pesticide exposure and lung cancer mortality in Leningrad province in Russia.

This study was carried out to examine the association between pesticide exposure and lung cancer mortality. We conducted an autopsy based case-control study in Leningrad Province in Russia. A total of 540 lung cancer cases and 582 controls were identified among subjects who had died in the hospitals of the Leningrad province between 1993 and 1998. Using work history records, we assessed exposure to pesticide at the level of industry and job title. Unconditional logistic regression was used to calculate adjusted odds ratio for pesticide exposure and lung cancer mortality. There was no association between ever exposure to pesticide and lung cancer mortality overall (odds ratio=1.06, 95% confidence interval=0.82-1.36) and in both men (odds ratio=1.11, 95% confidence interval=0.84-1.46) and women (odds ratio=0.74, 95% confidence interval=0.37-1.46). We observed no statistically significant odds ratio by duration of pesticide exposure, intensity of pesticide exposure, and cumulative pesticide exposures with lung cancer mortality in both smokers and nonsmokers. Odds ratio also did not differ when the analysis was restricted to individuals who had exposure data with high confidence scores. Our findings suggest no associations between pesticide exposures and mortality of lung cancer in the population of the Leningrad province in Russia that deserves further evaluation.

Aged↗