Biomedical subjects

Daniel Krewski

Publications and source records attributed to Daniel Krewski.

At least 19 recordsLinked to original sources

PubMed2026

Maternal vaccination with RSVpreF and risk of hypertensive disorders of pregnancy: a systematic review and meta-analysis.

BACKGROUND: A bivalent respiratory syncytial virus (RSV) prefusion F protein-based vaccine (RSVpreF) was approved in the United States in August 2023 for use during pregnancy to prevent infant RSV-associated lower respiratory tract disease. The pivotal phase 3 trial identified a numerical imbalance in hypertensive disorders of pregnancy (HDP) that did not reach statistical significance; postmarketing observational studies have since reported inconsistent findings. We conducted a systematic review and meta-analysis to assess this association. METHODS: We searched MEDLINE, Embase, CENTRAL, Scopus, ClinicalTrials.gov, and WHO ICTRP from inception to Jan 26, 2026, for randomized controlled trials (RCTs) and observational studies comparing HDP outcomes in RSVpreF-vaccinated versus unvaccinated or placebo-receiving pregnant individuals. Unadjusted risk ratios (RRs) were pooled using a random-effects model; adjusted estimates from observational studies were pooled separately by inverse variance methods. This study is registered with PROSPERO (CRD420251026835). RESULTS: Nine studies were included (3 RCTs, 6 retrospective cohort studies; n = 148,267). RSVpreF vaccination was associated with a small but statistically significant increase in overall HDP risk (RR 1·08, 95% CI 1·02-1·13; p = 0·004; I2 = 44%), driven by the observational studies group (1·08, 1·02-1·14; I2 = 61%); RCTs showed a directionally consistent but non-significant RR (1·12, 0·87-1·43; I2 = 0%). The association was attributable to gestational hypertension, with no significant association for preeclampsia/eclampsia. CONCLUSION: Maternal RSVpreF vaccination was associated with a small increase in HDP attributable to gestational hypertension and driven primarily by observational studies, in which residual confounding remains possible. The benefits of infant RSV prevention remain substantial, and these findings support continued postmarketing surveillance and informed shared decision-making.

Humans↗

PubMed2007

A comparison of methods for the analysis of recurrent health outcome data with environmental covariates.

Recurrent events such as repeated hospital admissions for the same health outcome occur frequently in environmental health studies. Dewanji and Moolgavkar proposed a flexible parametric model and a conditional likelihood analysis for recurrent events based on a Poisson process formulation. In this paper, we examine the statistical properties of the Dewanji-Moolgavkar (DM) estimator of the risk of an adverse health outcome associated with environmental exposures based on recurrent event data using computer simulation. We also compare the DM approach with both case-crossover analysis for multiple observations and time series analysis when there are no subject-specific covariates. When using a correctly specified model, the DM method produced better estimates with respect to relative mean square error when each subject had constant or curved baseline intensity functions than it did when baseline intensities were increasing or decreasing in a linear fashion. For under-specified models, the DM method outperformed case-crossover analysis for decreasing straight line intensity functions, was outperformed by case-crossover analysis for increasing straight line intensity functions, and was roughly equivalent to case-crossover analysis for constant and curved intensity functions. Case-crossover analysis produced superior risk estimates more frequently than the other two methods in the cases considered here, especially for linear representations of the baseline intensities.

Aged↗

PubMed2006

In utero pesticide exposure and childhood morbidity.

In humans, immune development begins early in embryonic life and continues throughout the early postnatal period. Although a number of pesticides have been observed to induce developmental immunotoxicity in mice, few human studies have examined the long term effects of in utero pesticide exposure on childhood morbidity. Empirical evidence suggests that the vulnerable period for toxic insults to the developing immune system extends from early gestation to adolescence in humans and animals. Using data from the Ontario Farm Family Health Study, we examined the relationship between farm couple exposures to pesticides during pregnancy and subsequent health outcomes in their offspring, including: persistent cough or bronchitis, asthma, and allergies or hayfever. No strong associations between pesticide exposures during pregnancy and persistent cough or bronchitis, or asthma were found. There was suggestive evidence that allergies and hayfever appeared to be more common in offspring, especially male offspring, exposed to certain specific pesticides during the period of pregnancy. Nevertheless, given the indirect indicators of pesticide exposure used in this study, and the scarcity of human studies on in utero exposure to pesticides and the development of allergies and other child health outcomes, these findings serve primarily to generate hypotheses for future research.

Adult↗

PubMed2006

Impacts of operative delivery for the first twin on neonatal outcomes in the second twin.

We assess the impacts of operative delivery for the first twins with vertex presentation on neonatal outcomes in second twins using the 1995 to 1997 twin registry data of the United States. A total of 102,554 eligible twin pairs with vertex presentation for the first twin were included in the analysis. Of these, 50,748 (49.5%) first twins had a normal vaginal delivery, 43,504 (42.4%) were delivered by cesarean section, and 8302 (8.1%) were delivered by vaginal operation (vacuum extraction or forceps). In term twins, the risks of asphyxia-related mortality (odds ratio [OR], 3.08; 95% CI, 1.07 to 8.45), newborn injury (OR, 2.10; 95% 1.39 to 3.12), low Apgar score at 5 minutes (OR, 1.49; 95% 1.24 to 1.78), and mechanical ventilation use (OR, 1.34; 95% 1.20 to 1.51) were increased in the second twins whose co-twins were delivered by vaginal operation compared with those whose co-twins who had normal vaginal delivery. In contrast, the risks of asphyxia-related mortality (OR, 0.55; 95% 0.17 to 1.57), newborn injury (OR, 0.20; 95% 0.11 to 0.34), low Apgar score at 5 minutes (OR, 0.51; 95% 0.44 to 0.60), and mechanical ventilation use (OR, 0.77; 95% 0.71 to 0.83) were decreased in the second twins whose co-twins were delivered by cesarean section compared with those whose co-twins had a normal vaginal delivery. In conclusion, vaginal operative delivery for the first twins is related to the adverse neonatal outcomes of their co-twins, whereas cesarean delivery for the first twins is associated with the beneficial neonatal outcomes of their co-twins.

Apgar Score↗

PubMed2006

Estimates of the cancer burden in Europe from radioactive fallout from the Chernobyl accident.

The Chernobyl accident, which occurred April 26, 1986, resulted in a large release of radionuclides, which were deposited over a very wide area, particularly in Europe. Although an increased risk of thyroid cancer in exposed children has been clearly demonstrated in the most contaminated regions, the impact of the accident on the risk of other cancers as well as elsewhere in Europe is less clear. The objective of the present study was to evaluate the human cancer burden in Europe as a whole from radioactive fallout from the accident. Average country- and region-specific whole-body and thyroid doses from Chernobyl were estimated using new dosimetric models and radiological data. Numbers of cancer cases and deaths possibly attributable to radiation from Chernobyl were estimated, applying state-of-the-art risk models derived from studies of other irradiated populations. Simultaneously, trends in cancer incidence and mortality were examined over time and by dose level. The risk projections suggest that by now Chernobyl may have caused about 1,000 cases of thyroid cancer and 4,000 cases of other cancers in Europe, representing about 0.01% of all incident cancers since the accident. Models predict that by 2065 about 16,000 (95% UI 3,400-72,000) cases of thyroid cancer and 25,000 (95% UI 11,000-59,000) cases of other cancers may be expected due to radiation from the accident, whereas several hundred million cancer cases are expected from other causes. Although these estimates are subject to considerable uncertainty, they provide an indication of the order of magnitude of the possible impact of the Chernobyl accident. It is unlikely that the cancer burden from the largest radiological accident to date could be detected by monitoring national cancer statistics. Indeed, results of analyses of time trends in cancer incidence and mortality in Europe do not, at present, indicate any increase in cancer rates -- other than of thyroid cancer in the most contaminated regions -- that can be clearly attributed to radiation from the Chernobyl accident.

Adolescent↗

PubMed2006

An overview of the association between allergy and cancer.

Numerous epidemiological studies have evaluated some aspect of the association between a history of allergy and cancer occurrence. In this article, an overview of the epidemiological evidence is presented with a discussion of a number of methodological issues important in this area of study. Literature searches were conducted using the MEDLINE database from 1966 through to August 2005 to identify articles that explored a personal history of allergic disorders as a risk factor for cancer. Although it is difficult to draw conclusions between allergy and cancer at many sites because of insufficient evidence or a lack of consistency both within and among studies completed to date, strong inverse associations have been reported for pancreatic cancer and glioma, whereas lung cancer was positively associated with asthma. Additional studies are needed to confirm these finding and to address the limitations of previous studies, including the validity and reliability of exposure measures and control for confounding. Further, large prospective studies using cancer incidence would be particularly useful, including studies using biological markers of allergic status to reduce potential misclassification and to confirm the results of previous studies based on self-report. There is also a need for further basic research to clarify a potential mechanism, should an association exist.

Brain Neoplasms↗

PubMed2006

The effects of recall errors and of selection bias in epidemiologic studies of mobile phone use and cancer risk.

This paper examines the effects of systematic and random errors in recall and of selection bias in case-control studies of mobile phone use and cancer. These sensitivity analyses are based on Monte-Carlo computer simulations and were carried out within the INTERPHONE Study, an international collaborative case-control study in 13 countries. Recall error scenarios simulated plausible values of random and systematic, non-differential and differential recall errors in amount of mobile phone use reported by study subjects. Plausible values for the recall error were obtained from validation studies. Selection bias scenarios assumed varying selection probabilities for cases and controls, mobile phone users, and non-users. Where possible these selection probabilities were based on existing information from non-respondents in INTERPHONE. Simulations used exposure distributions based on existing INTERPHONE data and assumed varying levels of the true risk of brain cancer related to mobile phone use. Results suggest that random recall errors of plausible levels can lead to a large underestimation in the risk of brain cancer associated with mobile phone use. Random errors were found to have larger impact than plausible systematic errors. Differential errors in recall had very little additional impact in the presence of large random errors. Selection bias resulting from underselection of unexposed controls led to J-shaped exposure-response patterns, with risk apparently decreasing at low to moderate exposure levels. The present results, in conjunction with those of the validation studies conducted within the INTERPHONE study, will play an important role in the interpretation of existing and future case-control studies of mobile phone use and cancer risk, including the INTERPHONE study.

Case-Control Studies↗

PubMed2006

Association between maternal exposure to ambient air pollutants during pregnancy and fetal growth restriction.

Previous research demonstrated consistent associations between ambient air pollution and emergency room visits, hospitalizations, and mortality. Effect of air pollution on perinatal outcomes has recently drawn more attention. We examined the association between intrauterine growth restriction (IUGR) among singleton term live births and sulfur dioxide (SO2), nitrogen dioxide (NO2), carbon monoxide (CO), ozone (O3), and fine particles (PM2.5) present in ambient air in the Canadian cities of Calgary, Edmonton, and Montreal for the period 1985-2000. Multiple logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for IUGR, based on average daily levels of individual pollutants over each month and trimester of pregnancy after adjustment for maternal age, parity, infant gender, season, and city of residence. A 1 ppm increase in CO was associated with an increased risk of IUGR in the first (OR=1.18; 95% CI 1.14-1.23), second (OR=1.15; 95% CI 1.10-1.19) and third (OR=1.19; 95% CI 1.14-1.24) trimesters of pregnancy, respectively. A 20 ppb increase in NO2 (OR=1.16; 95% CI 1.09-1.24; OR=1.14; 95% CI 1.06--1.21; and OR=1.16; 95% CI 1.09-1.24 in the first, second, and third trimesters) and a 10 mug/m3 increase in PM2.5 (OR=1.07; 95% CI 1.03-1.10; OR=1.06; 95% CI 1.03-1.10; and OR=1.06; 95% CI 1.03-1.10) were also associated with an increased risk of IUGR. Consistent results were found when ORs were calculated by month rather than trimester of pregnancy. Our findings add to the emerging body of evidence that exposure to relatively low levels of ambient air pollutants in urban areas during pregnancy is associated with adverse effects on fetal growth.

Air Pollutants↗

PubMed2006

Biologically based analysis of lung cancer incidence in a large Canadian occupational cohort with low-dose ionizing radiation exposure, and comparison with Japanese atomic bomb survivors.

Lung cancer incidence is analyzed in a large Canadian National Dose Registry (CNDR) cohort with individual annual dosimetry for low-dose occupational exposure to gamma and tritium radiation using the two-stage clonal expansion model (TSCE) and extensions of the model with up to 10 initiation steps. Models with clonal expansion turned off provide very poor fits and are rejected. Characteristic and distinct temporal patterns of excess relative risk (ERR) are found for dose response affecting early, middle, or late stages of carcinogenesis, that is, initiation with one or more stages, clonal expansion, or malignant conversion. Both fixed lag and lag distributions are used to model time from first malignant cell to incidence. Background rates are adjusted for gender and birth cohort. Lacking individual smoking data, surrogate annual smoking doses based on U.S. annual per capita cigarette consumption appear to account for much of the birth cohort effect, leaving radiation dose response relatively unchanged. The mean cumulative exposure for males receiving nonzero cumulative doses of gamma and tritium radiation was 18.2 mSv. The males have a significant dose response with 33 out of a total of 322 lung cancer cases attributable to radiation. There were 78 incident lung cancer among females, (with mean cumulative exposure of 3.8 mSv among females with nonzero exposure). The dose response for females appears smaller than for males but does not differ significantly from zero or from the male dose response. Findings for males include significant dose-response relationships for promotion and malignant conversion, but not initiation, and a protraction effect (sometimes called an inverse-dose-rate effect, where risk increases with protraction of a given dose). The dose response predicted by our analysis appears consistent with the risk for lung cancer incidence in the Japanese atomic bomb survivors cohort, provided that proper adjustments are made for duration of exposure and differences in background rate parameters.

Canada↗

PubMed2006

Association between air pollution and multiple respiratory hospitalizations among the elderly in Vancouver, Canada.

Recurrent events, such as repeated hospital admissions for the same health outcome, occur frequently in environmental health studies. In this study, we conducted an analysis of data on repeated respiratory hospitalizations among the elderly in Vancouver, Canada, for the period of June 1, 1995, to March 31, 1999, using a new method proposed by (Dewanji and Moolgavkar 2000, 2002) for recurrent events, and compared it with some traditional methods. In particular, we assessed the impact of ambient gaseous (SO2, NO2, CO, and O3) and particulate pollutants (PM10, PM2.5, and PM10-2.5) as well as the coefficient of haze (CoH) on recurrent respiratory hospital admissions. Using the new procedure, significant associations were found between admissions and 3-day, 5-day, and 7-day moving averages of the ambient SO2 concentrations, with the strongest association observed at the 7-day lag (RR = 1.044, 95% CI: 1.018-1.070). We also found PM10-2.5 for 3-day and 5-day lag to be significant, with the strongest association at 5-day lag (RR = 1.020, 95% CI: 1.001-1.039). No significant associations with admission were found with current day exposure.

Aged↗

PubMed2006

A combined analysis of North American case-control studies of residential radon and lung cancer.

Cohort studies have consistently shown underground miners exposed to high levels of radon to be at excess risk of lung cancer, and extrapolations based on those results indicate that residential radon may be responsible for nearly 10-15% of all lung cancer deaths per year in the United States. However, case-control studies of residential radon and lung cancer have provided ambiguous evidence of radon lung cancer risks. Regardless, alpha-particle emissions from the short-lived radioactive radon decay products can damage cellular DNA. The possibility that a demonstrated lung carcinogen may be present in large numbers of homes raises a serious public health concern. Thus, a systematic analysis of pooled data from all North American residential radon studies was undertaken to provide a more direct characterization of the public health risk posed by prolonged radon exposure. To evaluate the risk associated with prolonged residential radon exposure, a combined analysis of the primary data from seven large scale case-control studies of residential radon and lung cancer risk was conducted. The combined data set included a total of 4081 cases and 5281 controls, representing the largest aggregation of data on residential radon and lung cancer conducted to date. Residential radon concentrations were determined primarily by a-track detectors placed in the living areas of homes of the study subjects in order to obtain an integrated 1-yr average radon concentration in indoor air. Conditional likelihood regression was used to estimate the excess risk of lung cancer due to residential radon exposure, with adjustment for attained age, sex, study, smoking factors, residential mobility, and completeness of radon measurements. Although the main analyses were based on the combined data set as a whole, we also considered subsets of the data considered to have more accurate radon dosimetry. This included a subset of the data involving 3662 cases and 4966 controls with a-track radon measurements within the exposure time window (ETW) 5-30 yr prior to the index date considered previously by Krewski et al. (2005). Additional restrictions focused on subjects for which a greater proportion of the ETW was covered by measured rather than imputed radon concentrations, and on subjects who occupied at most two residences. The estimated odds ratio (OR) of lung cancer generally increased with radon concentration. The OR trend was consistent with linearity (p = .10), and the excess OR (EOR) was 0.10 per Bq/m3 with 95% confidence limits (-0.01, 0.26). For the subset of the data considered previously by Krewski et al. (2005), the EOR was 0.11 (0.00, 0.28). Further limiting subjects based on our criteria (residential stability and completeness of radon monitoring) expected to improve radon dosimetry led to increased estimates of the EOR. For example, for subjects who had resided in only one or two houses in the 5-30 ETW and who had a-track radon measurements for at least 20 yr of this 25-yr period, the EOR was 0.18 (0.02, 0.43) per 100 Bq/m3. Both estimates are compatible with the EOR of 0.12 (0.02, 0.25) per 100 Bq/m3 predicted by downward extrapolation of the miner data. Collectively, these results provide direct evidence of an association between residential radon and lung cancer risk, a finding predicted by extrapolation of results from occupational studies of radon-exposed underground miners.

Adult↗

PubMed2006

An overview of the North American residential radon and lung cancer case-control studies.

Lung cancer has held the distinction as the most common cancer type worldwide since 1985 (Parkin et al., 1993). Recent estimates suggest that lung cancer accounted for 1.2 million deaths worldwide in 2002, which represents 17.6% of the global cancer deaths (Parkin et al., 2005). During 2002, the highest lung cancer rates for men worldwide reportedly occurred in North America and Eastern Europe, whereas the highest rates in females occurred in North America and Northern Europe (Parkin et al., 2005). While tobacco smoking is the leading risk factor for lung cancer, because of the magnitude of lung cancer mortality, even secondary causes of lung cancer present a major public health concern (Field, 2001). Extrapolations from epidemiologic studies of radon-exposed miners project that approximately 18,600 lung cancer deaths per year (range 3000 to 41,000) in the United States alone are attributable to residential radon progeny exposure (National Research Council, 1999). Because of differences between the mines and the home environment, as well as differences (such as breathing rates) between miners and the general public, there was a need to directly evaluate effects of radon in homes. Seven major residential case-control radon studies have been conducted in North America to directly examine the association between prolonged radon progeny (radon) exposure and lung cancer. Six of the studies were performed in the United States including studies in New Jersey, Missouri (two studies), Iowa, and the combined states study (Connecticut, Utah, and southern Idaho). The seventh study was performed in Winnipeg, Manitoba, Canada. The residential case-control studies performed in the United States were previously reviewed elsewhere (Field, 2001). The goal of this review is to provide additional details regarding the methodologies and findings for the individual studies. Radon concentration units presented in this review adhere to the types (pCi/L or Bq/m3) presented in the individual studies. One picocurie per liter is equivalent to 37 Bq/m3. Because the Iowa study calculated actual measures of exposure (concentration x time), its exposures estimates are presented in the form WLM(5-19) (Field et al., 2000a). WLM(5-19) represents the working level months for exposures that occurred 5-19 yr prior to diagnosis for cases or time of interview for control. Eleven WLM(5-19) is approximately equivalent to an average residential radon exposure of 4 pCi/L for 15 yr, assuming a 70% home occupancy.

Air Pollutants, Radioactive↗

PubMed2006

Assessment and management of residential radon health risks: a report from the health Canada radon workshop.

Epidemiologic studies of uranium miners and other underground miners have consistently shown miners exposed to high levels of radon to be at increased risk of lung cancer. More recently, concern has arisen about lung cancer risks among people exposed to lower levels of radon in homes. The current Canadian guideline for residential radon exposure was set in 1988 at 800 Bq/m(3). Because of the accumulation of a considerable body of new scientific evidence on radon lung cancer risks since that time, Health Canada sponsored a workshop to review the current state-of-the-science on radon health risks. The specific objectives of the workshop were (1) to collect and assess scientific information relevant to setting national radon policy in Canada, and (2) to gather information on social, political, and operational considerations in setting national policy. The workshop, held on 3-4 March 2004, was attended by 38 invited scientists, regulators, and other stakeholders from Canada and the United States. The presentations on the first day dealt primarily with scientific issues. The combined analysis of North American residential radon and lung cancer studies was reviewed. The analysis confirmed a small but detectable increase in lung cancer risk at residential exposure levels. Current estimates suggest that radon in homes is responsible for approximately 10% of all lung cancer deaths in Canada, making radon the second leading cause of lung cancer after tobacco smoking. This was followed by a perspective from an UNSCEAR (United Nations Scientific Committee on the Effects of Atomic Radiation) working group on radon. There were two presentations on occupational exposures to radon and two presentations considered the possibility of radon as a causative factor for cardiovascular disease and for cancer in other organs besides the lung. The possible contribution of environmental tobacco smoke to lung cancers in nonsmokers was also considered. Areas for future research were identified. The second day was devoted to policy and operational issues. The presentations began with a perspective from the U.S. Environmental Protection Agency, followed by a history of radon policy development in Canada. Subsequent presentations dealt with the cost-effectiveness of radon mitigation, Canadian building codes and radon, and a summary of radon standards from around the world. Provincial representatives and a private consultant were given opportunities to present their viewpoints. A number of strategies for reducing residential radon exposure in Canada were recognized, including testing and mitigation of existing homes (on either a widespread or targeted basis) and changing the building code to require that radon mitigation devices be installed at the time a new home is constructed. The various elements of a comprehensive national radon policy were set forth.

Air Pollutants, Radioactive↗

PubMed2006

World Health Organization's International Radon Project.

Following initial in vitro and in vivo studies and important studies of uranium miners, scientists have now completed impressive case-control studies of lung cancer risk from exposure to residential radon. Researchers have pooled these studies, in which all the information from the individual studies was reanalyzed. These pooled analyzes confirm that in the context of residential exposure, radon is now an established risk factor for lung cancer. Many of the initial uncertainties have been reduced, and health risk assessors are now confident that radon may contribute to as much as 10% of the total burden of lung cancer--that is, 2% of all cancers in the population, worldwide. To reduce residential radon lung cancer risk, national authorities must have methods and tools based on solid scientific evidence and sound public health policies. To meet these needs, the World Health Organization (WHO) has initiated the WHO International Radon Project. This three year project, to be implemented during the period 2005-2008, will include (1) a worldwide database on national residential radon levels, radon action levels, regulations, research institutions, and authorities; (2) public health guidance for awareness-raising and mitigation; and (3) an estimation of the global burden of disease (GDB) associated with radon exposure.

Air Pollution, Indoor↗

PubMed2005

Maternal cigarette smoking and the risk of pregnancy-induced hypertension and eclampsia.

BACKGROUND: Although previous studies have found that maternal smoking decreases the risk of pregnancy-induced hypertension (PIH), the difference of this effect between primiparous and multiparous women has not been well studied and the results of the exposure-response relationships between maternal smoking and PIH are inconsistent. No previous study has specifically examined the relationship between maternal smoking and eclampsia. METHODS: We analysed data from a population-based retrospective cohort study of 3 153 944 singleton pregnancies in the US. The data were derived from the national linked birth/infant mortality database for 1998. Multiple logistic regressions were used to describe the relationship between cigarette smoking and PIH and eclampsia. RESULTS: The adjusted odds ratios (ORs) [95% confidence intervals (95% CIs)] for PIH were 0.80 (0.77-0.83) for primiparous women and 0.81 (0.78-0.83) for multiparous women among smokers compared with non-smokers. The corresponding adjusted ORs (95% CIs) for eclampsia were 0.74 (0.66-0.82) and 0.75 (0.68-0.83), respectively. For PIH, the adjusted OR (95% CI) for smokers vs non-smokers were 0.82 (0.79-0.86), 0.81 (0.78-0.83), 0.80 (0.77-0.83), and 0.88 (0.79-0.98), respectively, for 1-5, 6-10, 11-20, and >20 cigarettes per day (test for trend: P = 0.86). The corresponding figures for eclampsia were 0.85 (0.75-0.95), 0.74 (0.66-0.82), 0.68 (0.58-0.78), and 0.73 (0.49-1.04), respectively (test for trend: P = 0.02). CONCLUSION: Maternal cigarette smoking decreases the risk of PIH and eclampsia, with a significant inverse exposure-response relationship apparent for eclampsia.

Adolescent↗

PubMed2005

Epidemiology of testicular cancer: an overview.

Testicular cancer is a rare disease, accounting for 1.1% of all malignant neoplasms in Canadian males. Despite the low overall incidence of testicular cancer, it is the most common malignancy among young men. The incidence rate of testicular cancer has been increasing since the middle of the 20th century in many western countries. However, the etiology of testicular cancer is not well understood. A search of the peer-reviewed literature was conducted to identify important articles for review and inclusion in this overview of the epidemiology of testicular cancer. Most of the established risk factors are related to early life events, including cryptorchidism, carcinoma in situ and in utero exposure to estrogens. Occupational, lifestyle, socioeconomic and other risk factors have demonstrated mixed associations with testicular cancer. Although there are few established risk factors for testicular cancer, some appear to be related to hormonal balance at various life stages. Lifestyle and occupational exposures occurring later in life may play a role in promoting the disease, although they are not likely involved in cancer initiation. In addition to summarizing the current epidemiologic evidence on risk factors for testicular cancer, we suggest future research directions that may elucidate the etiology of testicular cancer.

Adult↗

PubMed2005

Environmental lead level and pregnancy-induced hypertension.

Previous studies have suggested that environmental lead exposure increases the risk of hypertension in the general population. In this article, the authors used the 1998 linked birth/infant death database of the United States to examine the association between environmental lead level and the occurrence of pregnancy-induced hypertension (PIH). Yearly summaries of environmental lead levels were abstracted from the US Environmental Protection Agency's air pollution databases, and linked with birth/infant death records by state codes. Generalized estimating equations (GEEs) were used to evaluate the odds ratios of PIH associated with environmental lead measured at ecological levels, with adjustment for maternal age, race, education level, marital status, parity, and adequacy of prenatal care measured at individual levels, stratified by maternal cigarette smoking. A total of 2,994,072 women pregnant in 1998 were included in this study. With the first quartile of lead level as the reference group, the odds ratio for PIH among all study subjects in the second quartile of seasonal average lead level at conception was 1.07 (95% CI: 1.05-1.08), and odds ratios in the third and fourth quartiles were 1.22 (95% CI: 1.20-1.25) and 1.16 (95% CI: 1.15-1.18), respectively. The odds ratios for the second, third, and fourth quartiles of seasonal average lead level at birth were 1.07 (95% CI: 1.05-1.09), 1.21 (95% CI: 1.19-1.23), and 1.15 (95% CI: 1.13-1.17), respectively. The risk of PIH increased by 4% per 0.05 microg/m3 increase in seasonal average lead level at conception and birth, in both smokers and nonsmokers. These results suggest that higher environmental lead levels increase the risk of PIH.

Adult↗

PubMed2005

Cancer mortality among US men and women with asthma and hay fever.

The relation between self-reported physician-diagnosed asthma and/or hay fever and cancer mortality was explored in a prospective cohort study of 1,102,247 US men and women who were cancer-free at baseline. During 18 years of follow-up, from 1982 to 2000, there were 81,114 cancer deaths. Cox proportional hazards models were used to obtain adjusted relative risks for all cancer mortality and for cancer mortality at 12 sites associated with allergy indicators. There were significant inverse associations between a history of both asthma and hay fever and overall cancer mortality (relative risk (RR) = 0.88, 95% confidence interval (CI): 0.83, 0.93) and colorectal cancer mortality (RR = 0.76, 95% CI: 0.64, 0.91) in comparison with persons with neither of these allergic conditions. A history of hay fever only was associated with a significantly lowered risk of pancreatic cancer mortality, and a history of asthma only was associated with a significantly lowered risk of leukemia mortality. In never smokers, these associations persisted but were no longer significant. Results for mortality from cancer at other sites were less consistent. Collectively, these results suggest an inverse association between a history of allergy and cancer mortality; however, the strength of evidence for this association is limited.

Adult↗