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N Jourenkova

Publications and source records attributed to N Jourenkova.

10 recordsLinked to original sources
PubMed2001

Risk of pancreatic cancer in workers exposed to chlorinated hydrocarbon solvents and related compounds: a meta-analysis.

This is a meta-analysis of occupational exposures to chlorinated hydrocarbon (CHC) solvents and pancreatic cancer, based primarily on studies that addressed exposure directly (agent studies) and secondarily on studies that reported data without verification of individual CHC exposures (job title studies), all of which were listed in databases for the period January 1969 to May 1998. Standardized extraction of data and double-checking of consistency of data extraction by five extractors were done. Simple random models estimated meta-relative risks. Suggestive weak excesses were found for trichloroethylene (meta-relative risk (MRR) = 1.24, 95% confidence interval (CI): 0.79, 1.97), polychlorinated biphenyls (MRR = 1.37, 95% CI: 0.56, 3.31), methylene chloride (MRR = 1.42, 95% CI: 0.80, 2.53), and vinyl chloride (MRR = 1.17, 95% CI: 0.71, 1.91) but not for carbon tetrachloride. One study addressed tetrachloroethylene (MRR = 3.08, 95% CI: 0.63, 8.99); another investigated chlorohydrin production (MRR = 4.92, 95% CI: 1.58, 11.4). Exposure-response meta-analyses for trichloroethylene and methylene chloride failed to reveal trends. Job title studies on metal degreasing and dry cleaning revealed significant MRRs (2.0 and 1.4, respectively). Publication bias was unlikely. Confounding may have remained insufficiently controlled. Unless the results are seriously biased by exposure or endpoint misclassification or by confounding, strong causal associations between CHC compounds and pancreatic cancer can be judged unlikely. Interactions between environmental and occupational agents, lifestyle factors, and genetic susceptibility remain a possibility, but the data for this meta-analysis did not address interactions.

Canada↗
PubMed2001

Metabolic genetic polymorphisms and susceptibility to lung cancer.

Activity of some enzymes implicated in the metabolism of tobacco carcinogens presents a great variability between individuals due to the existence of a polymorphism in gene coding for these enzymes. Individual susceptibility to develop lung cancer could therefore depend not only on exposure to tobacco smoking, but also on genetic capacity to activate or inactivate tobacco carcinogens. This article summarizes the state of knowledge on metabolic polymorphisms and lung cancer susceptibility, and opens the discussion on the future direction of this promising way of research.

Arylamine N-Acetyltransferase↗
PubMed2001

Glutathione S-transferase M1, M3, P1, and T1 genetic polymorphisms and susceptibility to breast cancer.

This study was undertaken to examine if glutathione S-transferase (GST) M1, M3, P1, and T1 genotypes affected breast cancer risk in Finnish women. The study population consisted of 483 incident breast cancer cases and 482 healthy population controls. Genotyping analyses were performed by PCR-based methods, and odds ratios (ORs) and 95% confidence intervals (CIs) were calculated by unconditional logistic regression adjusting for known or suspected risk factors for breast cancer. When the genes were studied separately, the only significant finding was between GSTM1 null genotype and postmenopausal breast cancer risk (OR, 1.49; 95% CI, 1.03-2.15). Conversely, when the potential combined effects of the at-risk genotypes were examined, significant associations were observed only among premenopausal women. Although only a moderate risk of breast cancer was seen for premenopausal women concurrently carrying the GSTM3*B allele containing genotypes and the GSTP1 Ile/ Ile genotype (OR, 2.07; 95% CI, 1.02-4.18), the risk rose steeply if they simultaneously lacked the GSTT1 gene (OR, 9.93, 95% CI, 1.10-90.0). A borderline significant increase in the risk of breast cancer was also seen for premenopausal women with the combination of GSTM1 null, GSTP1 Ile/Ile, and GSTT1 null genotypes (OR, 3.96; 95% CI, 0.99-15.8). Our findings support the view that GST genotypes contribute to the individual breast cancer risk, especially in certain combinations.

Adult↗
PubMed2001

Polymorphic catechol-O-methyltransferase gene and breast cancer risk.

We examined 483 Finnish breast cancer cases and 482 population controls to determine the potential effect of catechol-O-methyltransferase (COMT) genotype in individual susceptibility to breast cancer. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated by unconditional logistic regression after adjustment for known or suspected risk factors for breast cancer. When studied separately by menopausal status, the COMT-L allele-containing genotypes were inversely associated with premenopausal breast cancer, especially with advanced stage of the disease (OR, 0.44; 95% CI, 0.22-0.87). Among postmenopausal women a similar decreased risk was seen for local carcinoma associated with the COMT-LL genotype (OR, 0.55; 95% CI, 0.31-0.98). The lowest breast cancer risk was seen in the postmenopausal women with the COMT-LL genotype and low body-mass index ( 30 months) use of estrogen (OR, 4.02; 95% CI, 1.13-14.3), or with the COMT-L allele-containing genotypes and early age (<or=12 years) at menarche (OR, 8.59; 95% CI, 1.85-39.8). Our study, therefore, suggests that the COMT genotype may define a portion of the individual breast cancer susceptibility that is associated with reproductive events and hormone exposure even if it does not seem to be a major overall risk factor for this malignancy.

Aged↗
PubMed2000

Occupational exposures and pancreatic cancer: a meta-analysis.

OBJECTIVES: Consolidation of epidemiological data on pancreatic cancer and worksite exposures. METHODS: Publications during 1969-98 were surveyed. Studies without verified exposures were excluded. Meta-analyses were conducted on data from 92 studies covering 161 populations, with results for 23 agents or groups of agents. With a standard format, five epidemiologists extracted risk estimates and variables of the structure and quality of each study. The extracted data were centrally checked. Random meta-models were applied. RESULTS: Based on 20 populations, exposure to chlorinated hydrocarbon (CHC) solvents and related compounds was associated with a meta-risk ratio (MRR) of 1.4 (95% confidence interval (95% CI) 1.0 to 1.8). Nickel and nickel compounds were considered in four populations (1.9; 1.2 to 3.2). Excesses were found also for chromium and chromium compounds (1.4; 0.9 to 2.3), polycyclic aromatic hydrocarbons (PAHs) (1.5; 0.9 to 2.5), organochlorine insecticides (1.5; 0.6 to 3.7), silica dust (1.4; 0.9 to 2.0), and aliphatic and alicyclic hydrocarbon solvents (1.3; 0.8 to 2.8). Evidence on pancreatic carcinogenicity was weak or non-positive for the following agents: acrylonitrile (1.1; 0.0 to 6.2); arsenic (1.0; 0.6 to 1.5); asbestos (1.1; 0.9 to 1.5); diesel engine exhaust (1.0; 0.9 to 1.3); electromagnetic fields (1.1; 0.8 to 1.4); formaldehyde (0. 8; 0.5 to 1.0); flour dust (1.1; 0.3 to 3.2); cadmium and cadmium compounds (0.7; 0.4 to 1.4); gasoline (1.0; 0.8 to 1.2); herbicides (1.0; 0.8 to 1.3); iron and iron compounds (1.3; 0.7 to 2.5); lead and lead compounds (1.1; 0.8 to 1.5); man-made vitreous fibres (1.0; 0.6 to 1.6); oil mist (0.9; 0.8 to 1.0); and wood dust (1.1; 0.9 to 2.5). The occupational aetiological fraction of pancreatic cancer was estimated at 12%. In a subpopulation exposed to CHC solvents and related compounds, it was 29%; to chromium and chromium compounds, 23%; to nickel and nickel compounds, 47%; to insecticides, 33%; and to PAHs, 33%. CONCLUSION: Occupational exposures may increase risk of pancreatic cancer. High quality studies are called for on interactions between occupational, environmental, and lifestyle factors as well as interactions between genes and the environment.

Air Pollutants, Occupational↗
PubMed2000

Steroid metabolism gene CYP17 polymorphism and the development of breast cancer.

The potential role of the polymorphism in the CYP17 gene was evaluated in a case-control study with 483 incident breast cancer patients and 482 population controls, all of homogenous Finnish origin. Our data disagree with the earlier suggestions that the minor A2 variant of CYP17 would pose an increased risk for developing advanced breast cancer. In contrast, a tendency of inverse association was found for premenopausal women carrying the A2 allele containing genotypes with a multivariate adjusted odds ratio of 0.58 approaching statistical significance (95% CI, 0.31-1.07). Agreeing with previous observations, the protective effect of later age at menarche (> or =13 years) was mainly limited to women with A1/A1 genotype, although this could only be seen in premenopausal women (odds ratio, 0.34; 95% CI, 0.15-0.76). Similarly, we found a remarkably lower risk for premenopausal women with at least one child (odds ratio, 0.22; 95% CI, 0.07-0.62) to be mainly attributable to the A1/A1 genotype. CYP17 genotypes may thus modify individual breast cancer proneness in certain subpopulations, although they appear not to have any major modifying role in the risk of this malignancy overall. Because these findings are based on relatively small numbers in stratified analysis, they should, however, be interpreted with caution before being confirmed in future studies.

Adult↗
PubMed1998

Larynx cancer risk in relation to glutathione S-transferase M1 and T1 genotypes and tobacco smoking.

Glutathione S-transferase (GST) isoenzymes are involved in the detoxification of several tobacco smoke-derived carcinogens. It is thus conceivable that deficiency in GST activity due to homozygous deletion of the GSTM1 and GSTT1 genes (the null genotypes) may modulate susceptibility to smoking-induced cancers. The effects of the GSTM1 and GSTT1 null genotypes on laryngeal cancer risk were evaluated using peripheral blood DNA from 129 larynx cancer patients and 172 noncancer controls, all of whom were regular smokers. Increased larynx cancer risk was related to the GSTM1 null genotype [odds ratio (OR) = 1.6, 95% confidence interval (CI) = 1.0-2.8]. The OR associated with the GSTT1 null genotype was increased, although not significantly (OR = 1.4, 95% CI = 0.7-2.9). Individuals with concurrent lack of GSTM1 and GSTT1 genes had a doubled, although not significant, risk for larynx cancer when compared with those having at least one of these genes (OR = 2.0, 95% CI = 0.8-5.2) and had almost a 3-fold risk (OR = 2.7, 95% CI = 1.0-7.4) when compared with those with both genes. Moreover, a significant interaction between the GSTM1 genotype and levels of tobacco consumption (P < 0.05) was found; the GSTM1 null genotype was associated with an increased risk of larynx cancer among smokers of 20 g/day or less (OR = 2.9, 95% CI = 1.3-6.3) but not among heavier smokers (OR = 1.0; 95% CI = 0.5-2.0). In contrast, the GSTT1 null genotype posed an increased, although not significant, risk among long-term smokers (OR = 2.3, 95% CI = 0.9-5.4).

Aged↗
PubMed1997

Cancer risk from occupational and environmental exposure to polycyclic aromatic hydrocarbons.

Epidemiologic evidence on the relationship between polycyclic aromatic hydrocarbons (PAH) and cancer is reviewed. High occupational exposure to PAHs occurs in several industries and occupations. Covered here are aluminum production, coal gasification, coke production, iron and steel foundries, tar distillation, shale oil extraction, wood impregnation, roofing, road paving, carbon black production, carbon electrode production, chimney sweeping, and calcium carbide production. In addition, workers exposed to diesel engine exhaust in the transport industry and in related occupations are exposed to PAHs and nitro-PAHs. Heavy exposure to PAHs entails a substantial risk of lung, skin, and bladder cancer, which is not likely to be due to other carcinogenic exposures present in the same industries. The lung seems to be the major target organ of PAH carcinogenicity and increased risk is present in most of the industries and occupations listed above. An increased risk of skin cancer follows high dermal exposure. An increase in bladder cancer risk is found mainly in industries with high exposure to PAHs from coal tars and pitches. Increased risks have been reported for other organs, namely the larynx and the kidney; the available evidence, however, is inconclusive. The results of studies addressing environmental PAH exposure are consistent with these conclusions.

Acetylene↗