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Beate Ritz

Publications and source records attributed to Beate Ritz.

At least 19 recordsLinked to original sources
PubMed2006

Glutathione S-transferase mu, omega, pi, and theta class variants and smoking in Parkinson's disease.

GSTs are a family of inducible phase II enzymes that may play a neuroprotective role in Parkinson's disease (PD). GSTs may also modify PD risk by metabolizing compounds in cigarettes, as cigarette smoking is generally found to be associated with a decrease in PD risk. Using a population-based case-control study design, we examined polymorphisms of the mu, omega, pi, and theta classes of GST to elucidate the main effects and smoking-GST interactions on PD risk. From three rural California counties, we recruited 289 incident idiopathic PD cases, clinically confirmed by our study neurologist, and 270 population controls, marginally matched by age, gender, and race. We assessed main gene polymorphism associations and evaluated interactions between smoking and GST polymorphisms as departures from a multiplicative scale adjusting for age, gender, and race. We also restricted analyses to Caucasian subjects to address the potential for population stratification (n=235 cases, 220 controls). Among Caucasians, we observed a risk reduction in subjects carrying at least one variant allele for GSTO1 (OR=0.68, 95% CI: 0.47-0.98) and also GSTO2 (OR=0.64, 95% CI: 0.44-0.93); both genes were in strong linkage disequilibrium. No main gene effects were observed for the remaining polymorphisms. We noted a multiplicative interaction between ever having smoked regularly and GSTO1 (OR(interaction)=0.55, 95% CI: 0.33-0.92) and GSTO2 (OR(interaction)=0.54, 95% CI: 0.32-0.90). Results were similar when combining all races. These findings and the paucity of similar studies suggest a need for further inquiry into the association between GSTs, smoking, and PD risk.

Adult↗
PubMed2006

Effects of subchronic and chronic exposure to ambient air pollutants on infant bronchiolitis.

Ambient air pollutant exposure has been linked to childhood respiratory disease, but infants have received little study. The authors tested the hypotheses that subchronic and chronic exposure to fine particulate matter (particulate matter < or = 2.5 microm in aerodynamic diameter (PM2.5)), nitrogen dioxide, carbon monoxide, and ozone increases risk of severe infant bronchiolitis requiring hospitalization. Study subjects were derived from linked birth-hospital-discharge records of infants born in 1995-2000 in the South Coast Air Basin of California. Cases with a hospital discharge for bronchiolitis in infancy were matched to 10 age- and gestational-age-matched controls. Exposures in the month prior to hospitalization (subchronic) and mean lifetime exposure (chronic) referenced to the case diagnosis date were assessed on the basis of data derived from the California Air Resources Board. In conditional logistic regression, only subchronic and chronic PM2.5 exposures were associated with increased risk of bronchiolitis hospitalization after adjustment for confounders (per 10-microg/m3 increase, adjusted odds ratio = 1.09 (95% confidence interval: 1.04, 1.14) for both). Ozone was associated with reduced risk in the single-pollutant model, but this relation did not persist in multipollutant models including PM2.5. These unique US data suggest that infant bronchiolitis may be added to the list of adverse effects of PM2.5 exposure.

Air Pollutants↗
PubMed2006

Neural tube defects and maternal residential proximity to agricultural pesticide applications.

Residential proximity to applications of agricultural pesticides may be an important source of exposure to agents that have been classified as developmental toxins. Data on two case-control study populations of infants with neural tube defects (NTDs) and nonmalformed controls delivered in California between 1987 and 1991 were pooled to investigate whether maternal residential proximity to applications of specific pesticides or physicochemical groups of pesticides during early gestation increases the risk of these malformations. Maternal residential proximity within 1,000 m of pesticide applications was ascertained by linking mothers' addresses with agricultural pesticide use reports and crop maps. Odds ratios were computed by using conventional single- and multiple-pesticide and hierarchical multiple-pesticide logistic regression. In single-pesticide models, several pesticides were associated with NTDs after adjustment for study population, maternal ethnicity, educational level, cigarette smoking, and vitamin use. In a hierarchical multiple-pesticide model, effect estimates for only benomyl and methomyl suggested a possible association. Elevated risks of NTDs and anencephaly or spina bifida subtypes were also associated with exposures to chemicals classified as amide, benzimidazole, methyl carbamate, or organophosphorus pesticides and with increasing numbers of pesticides. These results suggest that ambient exposure to certain categories of agricultural pesticides may increase the risk of NTDs.

Adult↗
PubMed2006

Circulating melatonin levels: possible link between Parkinson's disease and cancer risk?

Lower rates of cancer mortality/incidence in patients with Parkinson's disease (PD) have given rise to speculations about risk or preventative factors common to both diseases, including life-style factors (such as smoking) and genetic susceptibility. Melatonin, a hormone known for its sleep regulatory effects, may play an important role in carcinogenesis as suggested by substantial laboratory and less direct epidemiologic evidence. Particularly, a reduction in melatonin, such as experienced by persons who are exposed to light at night, appears to increase cancer risk. Variations in melatonin levels have been linked to PD in several different ways. Some studies show higher morning melatonin levels in PD patients than in healthy controls. One could speculate that the sleep disorders that affect almost two thirds of those suffering from PD and can precede PD motor symptoms by several years may be associated with variations in melatonin levels. Moreover, in animal models, interventions that increase the bioavailability of melatonin appears to increase the severity of parkinsonian symptoms, whereas reduction in melatonin by pinealectomy or exposure to bright light can enhance recovery from parkinsonisms symptoms. Finally, preliminary epidemiological evidence suggests that longer years of working night shifts is associated with a reduced risk of PD among participants of the Nurses' Health Study (NHS), whereas longer hours of sleep appear to increase their risk. In sum, while lower melatonin concentrations may predict a higher cancer risk, there is also some evidence that they may be associated with a lower risk of PD. We therefore hypothesize that elevated circulating melatonin levels in PD patients may contribute to their lower cancer rates.

Animals↗
PubMed2006

Lack of replication of thirteen single-nucleotide polymorphisms implicated in Parkinson's disease: a large-scale international study.

BACKGROUND: A genome-wide association study identified 13 single-nucleotide polymorphisms (SNPs) significantly associated with Parkinson's disease. Small-scale replication studies were largely non-confirmatory, but a meta-analysis that included data from the original study could not exclude all SNP associations, leaving relevance of several markers uncertain. METHODS: Investigators from three Michael J Fox Foundation for Parkinson's Research-funded genetics consortia-comprising 14 teams-contributed DNA samples from 5526 patients with Parkinson's disease and 6682 controls, which were genotyped for the 13 SNPs. Most (88%) participants were of white, non-Hispanic descent. We assessed log-additive genetic effects using fixed and random effects models stratified by team and ethnic origin, and tested for heterogeneity across strata. A meta-analysis was undertaken that incorporated data from the original genome-wide study as well as subsequent replication studies. FINDINGS: In fixed and random-effects models no associations with any of the 13 SNPs were identified (odds ratios 0.89 to 1.09). Heterogeneity between studies and between ethnic groups was low for all SNPs. Subgroup analyses by age at study entry, ethnic origin, sex, and family history did not show any consistent associations. In our meta-analysis, no SNP showed significant association (summary odds ratios 0.95 to 1.08); there was little heterogeneity except for SNP rs7520966. INTERPRETATION: Our results do not lend support to the finding that the 13 SNPs reported in the original genome-wide association study are genetic susceptibility factors for Parkinson's disease.

Aged↗
PubMed2006

Validation of self-reported proximity to agricultural crops in a case-control study of neural tube defects.

Self-reported perinatal exposures to chemicals or pollutant sources in case-control studies of birth defects may be inaccurate due to misreporting among mothers. In a case-control study of neural tube defects delivered in California in 1987-1988, mothers of case and control infants were asked whether they lived within 0.25 mile (400 m) of agricultural crops. Responses were compared against a gold standard derived from historical agricultural land-use survey maps. The odds ratio for self-reported proximity to any crops (1.62, 95% confidence interval: 1.08, 2.43) appeared to be positively biased compared with the estimate for map-based proximity (1.17, 95% confidence interval: 0.79, 1.71). This pattern was also observed for proximity to specific crops such as nonpermanent and orchard crops. For vineyards, however, we observed an increased risk associated with map-based proximity (odds ratio=2.45, 95% confidence interval: 1.08, 5.58) but not with self-reported proximity (1.09, 95% confidence interval: 0.51, 2.34). The sensitivity of self-reported proximity to any crops was greater for case (65.7%) than control mothers (50.0%) while specificity was about the same for case and control mothers (87.5 vs. 89.3%), suggesting that control mothers under-reported proximity to crops. Differential reporting was also observed between geographic regions, urban and rural residents, and across levels of maternal employment and education. These results suggest differential reporting between case and control mothers as well as an influence from maternal demographic characteristics on reporting accuracy.

Adolescent↗
PubMed2006

Estimated effects of hydrazine exposure on cancer incidence and mortality in aerospace workers.

BACKGROUND: Animal studies suggest that hydrazine is a lung carcinogen, but human studies have been rare, rather small, and limited to cancer mortality. METHODS: We examined cancer mortality and incidence in a cohort of aerospace workers with varying exposure to hydrazine contained in rocket fuels-extending previous mortality follow-up from 1994 to 2001 and investigating cancer incidence for the period 1988-2000 using population-registry data. We newly estimated hydrazine effects adjusting for occupational exposures to other carcinogens assessed through a job-exposure matrix. Rate-ratio estimates were derived from Cox proportional hazards and random-effects models using time-dependent exposure measures for hydrazine adjusting for trichloroethylene, polycyclic aromatic hydrocarbons, benzene, and mineral oil exposures. RESULTS: Exposure to hydrazine was positively associated with lung cancer incidence (estimated rate ratio for high vs low exposure with 20-year lag = 2.5; 95% confidence interval = 1.3-4.9) and with colorectal cancer incidence (2.2; 1.0-4.6). Dose-response associations were observed for both outcomes; similar associations were found for lung cancer mortality but not for colorectal cancer mortality. Effect estimates for cancers of the pancreas, blood and lymph system, and kidneys were based on small numbers rendering our analyses uninformative, and patterns considering exposure levels and lags were inconsistent. Use of random-effect models did not change our results. CONCLUSIONS: The findings reported here are consistent with our previous results for lung cancer mortality; our new results suggest that exposure to hydrazine increases the risk of incident lung cancers. We also found, for the first time, an increased risk of colon cancers. Results for other cancer sites are inconclusive.

Aged↗
PubMed2006

Geographic model and biomarker-derived measures of pesticide exposure and Parkinson's disease.

For more than two decades, reports have suggested that pesticides and herbicides may be an etiologic factor in idiopathic Parkinson's disease (PD). To date, no clear associations with any specific pesticide have been demonstrated from epidemiological studies perhaps, in part, because methods of reliably estimating exposures are lacking. We tested the validity of a Geographic Information Systems (GIS)-based exposure assessment model that estimates potential environmental exposures at residences from pesticide applications to agricultural crops based on California Pesticide Use Reports (PUR). Using lipid-adjusted dichlorodiphenyldichloroethylene (DDE) serum levels as the "gold standard" for pesticide exposure, we conducted a validation study in a sample taken from an ongoing, population-based case-control study of PD in Central California. Residential, occupational, and other risk factor data were collected for 22 cases and 24 controls from Kern county, California. Environmental GIS-PUR-based organochlorine (OC) estimates were derived for each subject and compared to lipid-adjusted DDE serum levels. Relying on a linear regression model, we predicted log-transformed lipid-adjusted DDE serum levels. GIS-PUR-derived OC measure, body mass index, age, gender, mixing and loading pesticides by hand, and using pesticides in the home, together explained 47% of the DDE serum level variance (adjusted r(2) = 0.47). The specificity of using our environmental GIS-PUR-derived OC measures to identify those with high-serum DDE levels was reasonably good (87%). Our environmental GIS-PUR-based approach appears to provide a valid model for assessing residential exposures to agricultural pesticides.

California↗
PubMed2006

A case-crossover study of wintertime ambient air pollution and infant bronchiolitis.

UNLABELLED: We examined the association of infant bronchiolitis with acute exposure to ambient air pollutants. DESIGN: We employed a time-stratified case-crossover method and based the exposure windows on a priori, biologically based hypotheses. PARTICIPANTS: We evaluated effects in 19,901 infants in the South Coast Air Basin of California in 1995-2000 with a hospital discharge record for bronchiolitis in the first year of life (International Classification of Diseases, 9th Revision, CM466.1). EVALUATIONS/MEASUREMENTS: Study subjects' ZIP code was linked to ambient air pollution monitors to derive exposures. We estimated the risk of bronchiolitis hospitalization associated with increases in wintertime ambient air pollutants using conditional logistic regression. RESULTS: We observed no increased risk after acute exposure to particulate matter < or = 2.5 microm in aerodynamic diameter (PM2.5), carbon monoxide, or nitrogen dioxide. PM2.5 exposure models suggested a 26-41% increased risk in the most premature infants born at gestational ages between 25 and 29 weeks; however, these findings were based on very small numbers. CONCLUSIONS: We found little support for a link between acute increases in ambient air pollution and infant bronchiolitis except modestly increased risk for PM2.5 exposure among infants born very prematurely. In these infants, the periods of viral acquisition and incubation concurred with the time of increased risk. RELEVANCE TO PROFESSIONAL PRACTICE: We present novel data for the infant period and the key respiratory disease of infancy, bronchiolitis. Incompletely explained trends in rising bronchiolitis hospitalization rates and increasing number of infants born prematurely underscore the importance of evaluating the impact of ambient air pollution in this age group in other populations and studies.

Air Pollutants↗
PubMed2006

Air pollution and infant death in southern California, 1989-2000.

OBJECTIVE: We evaluated the influence of outdoor air pollution on infant death in the South Coast Air Basin of California, an area characterized by some of the worst air quality in the United States. METHODS: Linking birth and death certificates for infants who died between 1989 and 2000, we identified all infant deaths, matched 10 living control subjects to each case subject, and assigned the nearest air monitoring station to each birth address. For all subjects, we calculated average carbon monoxide, nitrogen dioxide, ozone, and particulate matter < 10 microm in aerodynamic diameter exposures experienced during the 2-week, 1-month, 2-month, and 6-month periods before a case subject's death. RESULTS: The risk of respiratory death increased from 20% to 36% per 1-ppm increase in average carbon monoxide levels 2 weeks before death in early infancy (age: 28 days to 3 months). We also estimated 7% to 12% risk increases for respiratory deaths per 10-microg/m3 increase in particulate matter < 10 microm in aerodynamic diameter exposure experienced 2 weeks before death for infants 4 to 12 months of age. Risk of respiratory death more than doubled for infants 7 to 12 months of age who were exposed to high average levels of particulates in the previous 6 months. Furthermore, the risk of dying as a result of sudden infant death syndrome increased 15% to 19% per 1-part per hundred million increase in average nitrogen dioxide levels 2 months before death. Low birth weight and preterm infants seemed to be more susceptible to air pollution-related death resulting from these causes; however, we lacked statistical power to confirm this heterogeneity with formal testing. CONCLUSIONS: Our results add to the growing body of literature implicating air pollution in infant death from respiratory causes and sudden infant death syndrome and provide additional information for future risk assessment.

Air↗
PubMed2005

Gain-of-function haplotypes in the vesicular monoamine transporter promoter are protective for Parkinson disease in women.

The vesicular monoamine transporter can protect against toxins that induce an acute parkinsonian syndrome. It has been hypothesized that cytoplasmic dopamine has subacute toxic effects in Parkinson Disease (PD) leading to neuronal death and clinical symptoms. Regulatory polymorphisms in the brain form of the vesicular monoamine transporter (VMAT2) which affect its quantitative expression might therefore serve as genetic risk factors for PD. We have screened the promoter region of the gene for VMAT2 (SLC18A2) and identified several novel polymorphisms that form discrete haplotypes. We have tested the common halpotypes in SLC18A2 for functional effects in reporter gene assays and found that there are several gain-of-function haplotypes that display significantly increased transcriptional activity from the reference element. These gain-of-function haplotypes were tested for association with PD and found to confer a protective effect that was selective for females. This finding is consistent with the prediction that increased sequestration of dopamine in secretory vesicles by VMAT2 is protective for PD.

Black or African American↗
PubMed2005

Preterm birth: the interaction of traffic-related air pollution with economic hardship in Los Angeles neighborhoods.

Preterm birth may be affected by the interaction of residential air pollution with neighborhood economic hardship. The authors examined variations in traffic-related pollution exposure--measured by distance-weighted traffic density--using a framework reflecting the social and physical environments. An adverse social environment was conceptualized as low socioeconomic status (SES) neighborhoods--census tracts with concentrated poverty, unemployment, and dependence on public assistance. An adverse physical environment was depicted by the winter season, when thermal inversions trap motor vehicle pollutants, thereby increasing traffic-related air pollution. Los Angeles County, California, birth records from 1994 to 1996 were linked to traffic counts, census data, and ambient air pollution measures. The authors fit multivariate logistic models of preterm birth, stratified by neighborhood SES and third pregnancy trimester season. Traffic-related air pollution exposure disproportionately affected low SES neighborhoods in the winter. Further, in these poorer neighborhoods, the winter season evidenced increased susceptibility among women with known risk factors. Health insurance was most beneficial to women residing in neighborhoods exposed to economic hardship and an adverse physical environment. Reducing preterm births warrants a concerted effort of social, economic, and environmental policies, focused on not only individual risk factors but also the reduction of localized air pollution, expansion of health-care coverage, and improvement of neighborhood resources.

Adolescent↗
PubMed2005

Radiotherapy for oral cancer as a risk factor for second primary cancers.

Radiation exposure, known to cause DNA damage, may be a potential source of field cancerization of the upper aerodigestive tract. Radiotherapy for head and neck cancers has been examined as a possible risk factor for second primary cancers, but the results have been equivocal. We evaluated the impact of therapeutic radiation for oral cancer on the risk of second primary cancers with data from the Surveillance, Epidemiology, and End Results (SEER) program for 1973-1999. Among 30,221 first primary oral squamous cell carcinoma patients, 6163 (20.4%) patients developed a second primary cancer, 5042 of which were metachronous. Patients treated with radiation only (RR=1.64, 95%CI=1.18-2.29) or radiation with surgery (RR=1.49, 95%CI=1.07, 2.06) had elevated risks of developing a second primary tumor, whereas patients treated with surgery only did not appear to be at increased risk (RR=1.28, 95%CI=0.93, 1.76). Consistent with an expected latent period between radiation exposure and tumor occurrence, radiation became a risk factor after 10 years of follow-up for solid cancers of the oral cavity (RR=2.8, 95%CI=1.5, 5.2), pharynx (RR=5.9, 95%CI=1.7, 20.7), esophagus (RR=3.9, 95%CI=1.1, 13.4) and lung (RR=1.5, 95%CI=1.0, 2.4), and after 1-5 years of follow-up for second primary leukemia (RR=2.5, 95%CI=1.0, 6.7). Radiotherapy for oral cancer appears to be a risk factor for second primary tumors. Further studies that account for chemotherapy and examine frequency and duration of radiotherapy would be of interest in confirming the observed association.

Aged↗
PubMed2005

Estimated effects of solvents and mineral oils on cancer incidence and mortality in a cohort of aerospace workers.

BACKGROUND: A retrospective cohort study of workers employed at a California aerospace company between 1950 and 1993 was conducted; it examined cancer mortality from exposures to the rocket fuel hydrazine. METHODS: In this study, we employed a job exposure matrix (JEM) to assess exposures to other known or suspected carcinogens-including trichloroethylene (TCE), polycyclic aromatic hydrocarbons (PAHs), mineral oils, and benzene-on cancer mortality (1960-2001) and incidence (1988-2000) in 6,107 male workers. We derived rate- (hazard-) ratios estimates from Cox proportional hazard models with time-dependent exposures. RESULTS: High levels of TCE exposure were positively associated with cancer incidence of the bladder (rate ratio (RR): 1.98, 95% confidence interval (CI) 0.93-4.22) and kidney (4.90; 1.23-19.6). High levels of exposure to mineral oils increased mortality and incidence of lung cancer (1.56; 1.02-2.39 and 1.99; 1.03-3.85), and incidence of melanoma (3.32; 1.20-9.24). Mineral oil exposures also contributed to incidence and mortality of esophageal and stomach cancers and of non-Hodgkin's lymphoma and leukemia when adjusting for other chemical exposures. Lagging exposure measures by 20 years changed effect estimates only minimally. No associations were observed for benzene or PAH exposures in this cohort. CONCLUSIONS: Our findings suggest that these aerospace workers who were highly exposed to mineral oils experienced an increased risk of developing and/or dying from cancers of the lung, melanoma, and possibly from cancers of the esophagus and stomach and non-Hodgkin's lymphoma and leukemia. These results and the increases we observed for TCE and kidney cancers are consistent with findings of previous studies.

Adult↗
PubMed2005

Clinical characteristics in early Parkinson's disease in a central California population-based study.

There is considerable variation in the phenotypic appearance of individuals with idiopathic Parkinson's disease (PD), which may translate into differences in disease progression in addition to underlying disease etiology. In this publication, we report on the demographic and clinical characteristics of 162 individuals diagnosed with clinically probable PD from January 1998 to June 2003 who resided in predominantly rural communities in central California. The majority of the subjects were Caucasian, male, and between 60 and 79 years of age. The akinetic-rigid and tremor-dominant subtypes were more common than the mixed subtype. The majority of subjects displayed motor signs of rigidity (92.0%), bradykinesia (95.7%), and gait problems (87.0%), whereas less than half (43.3%) of the subjects displayed a tremor. Three fourths of patients received a Hoehn and Yahr Scale score of Stage 2 or higher. One third of the patients were treated with levodopa, and patients under 60 years of age were more likely to be treated with dopamine agonists. Within 3 years after first diagnosis, 13% of subjects showed some signs of depression and 17% of subjects met criteria for mild dementia. Among our subjects, 17.3% reported a family history of PD in first- or second-degree relatives,15.4% a family history of essential tremor, and 14.2% of Alzheimer's disease. This study represents the most extensive phenotypic description of rural U.S. residents in the initial stages of PD who were recruited in a population-based manner; future follow-up may provide valuable information regarding the prognostic indication of these symptoms/signs and improve our understanding of the underlying etiology of PD.

Age of Onset↗