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Frank E Speizer

Publications and source records attributed to Frank E Speizer.

At least 19 recordsLinked to original sources

Extended work duration and the risk of self-reported percutaneous injuries in interns.

CONTEXT: In their first year of postgraduate training, interns commonly work shifts that are longer than 24 hours. Extended-duration work shifts are associated with increased risks of automobile crash, particularly during a commute from work. Interns may be at risk for other occupation-related injuries. OBJECTIVE: To assess the relationship between extended work duration and rates of percutaneous injuries in a diverse population of interns in the United States. DESIGN, SETTING, AND PARTICIPANTS: National prospective cohort study of 2737 of the estimated 18,447 interns in US postgraduate residency programs from July 2002 through May 2003. Each month, comprehensive Web-based surveys that asked about work schedules and the occurrence of percutaneous injuries in the previous month were sent to all participants. Case-crossover within-subjects analyses were performed. MAIN OUTCOME MEASURES: Comparisons of rates of percutaneous injuries during day work (6:30 am to 5:30 pm) after working overnight (extended work) vs day work that was not preceded by working overnight (nonextended work). We also compared injuries during the nighttime (11:30 pm to 7:30 am) vs the daytime (7:30 am to 3:30 pm). RESULTS: From a total of 17,003 monthly surveys, 498 percutaneous injuries were reported (0.029/intern-month). In 448 injuries, at least 1 contributing factor was reported. Lapse in concentration and fatigue were the 2 most commonly reported contributing factors (64% and 31% of injuries, respectively). Percutaneous injuries were more frequent during extended work compared with nonextended work (1.31/1000 opportunities vs 0.76/1000 opportunities, respectively; odds ratio [OR], 1.61; 95% confidence interval [CI], 1.46-1.78). Extended work injuries occurred after a mean of 29.1 consecutive work hours; nonextended work injuries occurred after a mean of 6.1 consecutive work hours. Injuries were more frequent during the nighttime than during the daytime (1.48/1000 opportunities vs 0.70/1000 opportunities, respectively; OR, 2.04; 95% CI, 1.98-2.11). CONCLUSION: Extended work duration and night work were associated with an increased risk of percutaneous injuries in this study population of physicians during their first year of clinical training.

Accidents, Occupational↗

Reduction in fine particulate air pollution and mortality: Extended follow-up of the Harvard Six Cities study.

RATIONALE: A large body of epidemiologic literature has found an association of increased fine particulate air pollution (PM2.5) with acute and chronic mortality. The effect of improvements in particle exposure is less clear. OBJECTIVES: Earlier analysis of the Harvard Six Cities adult cohort study showed an association between long-term ambient PM2.5 and mortality between enrollment in the mid-1970s and follow-up until 1990. We extended mortality follow-up for 8 yr in a period of reduced air pollution concentrations. METHODS: Annual city-specific PM2.5 concentrations were measured between 1979 and 1988, and estimated for later years from publicly available data. Exposure was defined as (1) city-specific mean PM2.5 during the two follow-up periods, (2) mean PM2.5 in the first period and change between these periods, (3) overall mean PM2.5 across the entire follow-up, and (4) year-specific mean PM2.5. Mortality rate ratios were estimated with Cox proportional hazards regression controlling for individual risk factors. MEASUREMENTS AND MAIN RESULTS: We found an increase in overall mortality associated with each 10 microg/m3 increase in PM2.5 modeled either as the overall mean (rate ratio [RR], 1.16; 95% confidence interval [CI], 1.07-1.26) or as exposure in the year of death (RR, 1.14; 95% CI, 1.06-1.22). PM2.5 exposure was associated with lung cancer (RR, 1.27; 95% CI, 0.96-1.69) and cardiovascular deaths (RR, 1.28; 95% CI, 1.13-1.44). Improved overall mortality was associated with decreased mean PM2.5 (10 microg/m3) between periods (RR, 0.73; 95% CI, 0.57-0.95). CONCLUSION: Total, cardiovascular, and lung cancer mortality were each positively associated with ambient PM2.5 concentrations. Reduced PM2.5 concentrations were associated with reduced mortality risk.

Adult↗

Increased risk of paroxysmal atrial fibrillation episodes associated with acute increases in ambient air pollution.

OBJECTIVES: We reported previously that 24-hr moving average ambient air pollution concentrations were positively associated with ventricular arrhythmias detected by implantable cardioverter defibrillators (ICDs). ICDs also detect paroxysmal atrial fibrillation episodes (PAF) that result in rapid ventricular rates. In this same cohort of ICD patients, we assessed the association between ambient air pollution and episodes of PAF. DESIGN: We performed a case-crossover study. PARTICIPANTS: Patients who lived in the Boston, Massachusetts, metropolitan area and who had ICDs implanted between June 1995 and December 1999 (n=203) were followed until July 2002. EVALUATIONS/MEASUREMENTS: We used conditional logistic regression to explore the association between community air pollution and 91 electrophysiologist-confirmed episodes of PAF among 29 subjects. RESULTS: We found a statistically significant positive association between episodes of PAF and increased ozone concentration (22 ppb) in the hour before the arrhythmia (odds ratio=2.08; 95% confidence interval=1.22, 3.54; p=0.001). The risk estimate for a longer (24-hr) moving average was smaller, thus suggesting an immediate effect. Positive but not statistically significant risks were associated with fine particles, nitrogen dioxide, and black carbon. CONCLUSIONS: Increased ambient O3 pollution was associated with increased risk of episodes of rapid ventricular response due to PAF, thereby suggesting that community air pollution may be a precipitant of these events.

Aged↗

Impact of extended-duration shifts on medical errors, adverse events, and attentional failures.

BACKGROUND: A recent randomized controlled trial in critical-care units revealed that the elimination of extended-duration work shifts (> or =24 h) reduces the rates of significant medical errors and polysomnographically recorded attentional failures. This raised the concern that the extended-duration shifts commonly worked by interns may contribute to the risk of medical errors being made, and perhaps to the risk of adverse events more generally. Our current study assessed whether extended-duration shifts worked by interns are associated with significant medical errors, adverse events, and attentional failures in a diverse population of interns across the United States. METHODS AND FINDINGS: We conducted a Web-based survey, across the United States, in which 2,737 residents in their first postgraduate year (interns) completed 17,003 monthly reports. The association between the number of extended-duration shifts worked in the month and the reporting of significant medical errors, preventable adverse events, and attentional failures was assessed using a case-crossover analysis in which each intern acted as his/her own control. Compared to months in which no extended-duration shifts were worked, during months in which between one and four extended-duration shifts and five or more extended-duration shifts were worked, the odds ratios of reporting at least one fatigue-related significant medical error were 3.5 (95% confidence interval [CI], 3.3-3.7) and 7.5 (95% CI, 7.2-7.8), respectively. The respective odds ratios for fatigue-related preventable adverse events, 8.7 (95% CI, 3.4-22) and 7.0 (95% CI, 4.3-11), were also increased. Interns working five or more extended-duration shifts per month reported more attentional failures during lectures, rounds, and clinical activities, including surgery and reported 300% more fatigue-related preventable adverse events resulting in a fatality. CONCLUSIONS: In our survey, extended-duration work shifts were associated with an increased risk of significant medical errors, adverse events, and attentional failures in interns across the United States. These results have important public policy implications for postgraduate medical education.

Adult↗

The SERPINE2 gene is associated with chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease (COPD) is a complex human disease likely influenced by multiple genes, cigarette smoking, and gene-by-smoking interactions, but only severe alpha 1-antitrypsin deficiency is a proven genetic risk factor for COPD. Prior linkage analyses in the Boston Early-Onset COPD Study have demonstrated significant linkage to a key intermediate phenotype of COPD on chromosome 2q. We integrated results from murine lung development and human COPD gene-expression microarray studies with human COPD linkage results on chromosome 2q to prioritize candidate-gene selection, thus identifying SERPINE2 as a positional candidate susceptibility gene for COPD. Immunohistochemistry demonstrated expression of serpine2 protein in mouse and human adult lung tissue. In family-based association testing of 127 severe, early-onset COPD pedigrees from the Boston Early-Onset COPD Study, we observed significant association with COPD phenotypes and 18 single-nucleotide polymorphisms (SNPs) in the SERPINE2 gene. Association of five of these SNPs with COPD was replicated in a case-control analysis, with cases from the National Emphysema Treatment Trial and controls from the Normative Aging Study. Family-based and case-control haplotype analyses supported similar regions of association within the SERPINE2 gene. When significantly associated SNPs in these haplotypic regions were included as covariates in linkage models, LOD score attenuation was observed most markedly in a smokers-only linkage model (LOD 4.41, attenuated to 1.74). After the integration of murine and human microarray data to inform candidate-gene selection, we observed significant family-based association and independent replication of association in a case-control study, suggesting that SERPINE2 is a COPD-susceptibility gene and is likely influenced by gene-by-smoking interaction.

Amyloid beta-Protein Precursor↗

A functional mutation in the terminal exon of elastin in severe, early-onset chronic obstructive pulmonary disease.

We describe a novel variant in the terminal exon of human elastin, c.2318 G > A, resulting in an amino acid substitution of glycine 773 to aspartate (G773D) in a pedigree with severe early-onset chronic obstructive pulmonary disease (COPD). Transfection studies with elastin cDNAs demonstrate that the glycine to aspartate change compromises the ability of the mutant protein to undergo normal elastin assembly. Other functional consequences of this amino acid substitution include altered proteolytic susceptibility of the C-terminal region of elastin and reduced interaction of the exon 36 sequence with matrix receptors on cells. These results suggest that the G773D variant confers structural and functional consequences relevant to the pathogenesis of COPD.

Alternative Splicing↗

Association of short-term ambient air pollution concentrations and ventricular arrhythmias.

The authors evaluated the association between ventricular arrhythmias detected by implantable cardioverter defibrillators and ambient air pollution concentrations in the hours immediately before the arrhythmia. Patients given implantable cardioverter defibrillators at the New England Medical Center in Boston, Massachusetts, between mid-1995 and 1999 who lived within 40 km of a central monitoring site (n = 203) were followed until July 2002. The authors used a case-crossover design to study the association between ambient air pollution and up to 798 confirmed ventricular arrhythmias among 84 subjects. The authors found that interquartile range increases in 24-hour moving average particulate matter less than 2.5 mum in aerodynamic diameter and ozone were associated with 19% and 21% increased risks of ventricular arrhythmia, respectively. For each, there was evidence of a linear exposure response, and the associations appeared independent. These associations were stronger than associations with mean concentrations on the same calendar day and previous calendar days. The authors did not find associations with pollutant concentrations less than 24 hours before the arrhythmia. Cases with a prior ventricular arrhythmia within 72 hours had greater risk associated with air pollutants than did cases without a recent arrhythmia. These results confirm previous findings and suggest that matching of pollution periods to arrhythmias is important in detecting such associations.

Aged↗

Attempted replication of reported chronic obstructive pulmonary disease candidate gene associations.

Case-control studies have successfully identified many significant genetic associations for complex diseases, but lack of replication has been a criticism of case-control genetic association studies in general. We selected 12 candidate genes with reported associations to chronic obstructive pulmonary disease (COPD) and genotyped 29 polymorphisms in a family-based study and in a case-control study. In the Boston Early-Onset COPD Study families, significant associations with quantitative and/or qualitative COPD-related phenotypes were found for the tumor necrosis factor (TNF)-alpha -308G>A promoter polymorphism (P < 0.02), a coding variant in surfactant protein B (SFTPB Thr131Ile) (P = 0.03), and the (GT)(31) allele of the heme oxygenase (HMOX1) promoter short tandem repeat (P = 0.02). In the case-control study, the SFTPB Thr131Ile polymorphism was associated with COPD, but only in the presence of a gene-by-environment interaction term (P = 0.01 for both main effect and interaction). The 30-repeat, but not the 31-repeat, allele of HMOX1 was associated (P = 0.04). The TNF -308G>A polymorphism was not significant. In addition, the microsomal epoxide hydrolase "fast" allele (EPHX1 His139Arg) was significantly associated in the case-control study (P = 0.03). Although some evidence for replication was found for SFTPB and HMOX1, none of the previously published COPD genetic associations was convincingly replicated across both study designs.

Adult↗

Extended work shifts and the risk of motor vehicle crashes among interns.

BACKGROUND: Long work hours and work shifts of an extended duration (> or =24 hours) remain a hallmark of medical education in the United States. Yet their effect on health and safety has not been evaluated with the use of validated measures. METHODS: We conducted a prospective nationwide, Web-based survey in which 2737 residents in their first postgraduate year (interns) completed 17,003 monthly reports that provided detailed information about work hours, work shifts of an extended duration, documented motor vehicle crashes, near-miss incidents, and incidents involving involuntary sleeping. RESULTS: The odds ratios for reporting a motor vehicle crash and for reporting a near-miss incident after an extended work shift, as compared with a shift that was not of extended duration, were 2.3 (95 percent confidence interval, 1.6 to 3.3) and 5.9 (95 percent confidence interval, 5.4 to 6.3), respectively. In a prospective analysis, every extended work shift that was scheduled in a month increased the monthly risk of a motor vehicle crash by 9.1 percent (95 percent confidence interval, 3.4 to 14.7 percent) and increased the monthly risk of a crash during the commute from work by 16.2 percent (95 percent confidence interval, 7.8 to 24.7 percent). In months in which interns worked five or more extended shifts, the risk that they would fall asleep while driving or while stopped in traffic was significantly increased (odds ratios, 2.39 [95 percent confidence interval, 2.31 to 2.46] and 3.69 [95 percent confidence interval, 3.60 to 3.77], respectively). CONCLUSIONS: Extended-duration work shifts, which are currently sanctioned by the Accreditation Council for Graduate Medical Education, pose safety hazards for interns. These results have implications for medical residency programs, which routinely schedule physicians to work more than 24 consecutive hours.

Accidents, Traffic↗

A prospective study of body mass index, hypertension, and smoking and the risk of renal cell carcinoma (United States).

OBJECTIVE: We prospectively investigated the independent association of hypertension, thiazide use, body mass index, weight change, and smoking with the risk of renal cell carcinoma among men and women using biennial mailed questionnaires. METHODS: The study population included 118,191 women participating in the Nurses' Health Study and 48,953 men participating in the Health Professionals Follow-up Study. RESULTS: During 24 years of follow-up for women and 12 years for men, 155 and 110 incident cases of renal cell carcinoma were confirmed, respectively. In multivariate models including age, body mass index (BMI), smoking and hypertension, higher BMI was confirmed as a risk factor for women and smoking as a risk factor for men and women. After adjusting for age, updated BMI and smoking, an updated diagnosis of hypertension was associated with renal cell carcinoma (RCC); the relative risk (RR) was 1.9 (95% CI 1.4-2.7) for women and 1.8 (95% CI 1.2-2.7) for men. Based on limited data regarding the use of thiazide diuretics, we did not observe a risk associated with their use, independent of the diagnosis of hypertension. CONCLUSIONS: Diagnosis of hypertension, higher BMI, and increasing pack-years of smoking appear to independently increase the risk of renal cell carcinoma.

Adult↗

Genome-wide linkage of forced mid-expiratory flow in chronic obstructive pulmonary disease.

Familial aggregation of forced expiratory flow during the middle half of the FVC (FEF(25-75%)) and FEF(25-75%)/FVC has been observed in the Boston Early-Onset Chronic Obstructive Pulmonary Disease Study, but linkage results have not been reported for these phenotypes. An autosomal whole genome-wide linkage scan was performed in 72 pedigrees ascertained through a proband with severe, early-onset chronic obstructive pulmonary disease, and linkage analyses of FEF(25-75%) and FEF(25-75%)/FVC were performed using Sequential Oligogenic Linkage Analysis Routines. There was suggestive evidence for linkage of FEF(25-75%)/FVC with chromosome 2 (LOD 2.60 at 216 cM). In a smokers-only analysis, evidence for linkage was observed for postbronchodilator FEF(25-75%) with chromosome 12 (LOD 5.03 at 35 cM) and chromosomes 2 and 12 for FEF(25-75%)/FVC (LOD 4.12 at 221 cM and LOD 3.46 at 35 cM, respectively); in the smokers-only model, evidence for linkage also was robust for FEV(1)/FVC on chromosome 2 (LOD 4.13 at 229 cM) and FEV(1) on chromosome 12 (LOD 3.26 at 36 cM). Our analyses provide evidence for linkage of FEF(25-75%) and FEF(25-75%)/FVC on chromosomes 2q and 12p. LOD scores of greater than two were also observed for chromosomes 16, 20, and 22 with the smokers-only analysis, which may suggest gene-by-smoking interactions in these regions.

Adult↗

A prospective study of dietary lactose and ovarian cancer.

The milk sugar lactose is an hypothesized risk factor for epithelial ovarian cancer because of possible direct toxic effects of its metabolites on oocytes or by compensatory gonadotropin stimulation. Women are presently encouraged to consume dairy products as a source of calcium to prevent osteoporosis. The objective of our study was to prospectively assess lactose, milk and milk product consumption in relation to ovarian cancer risk among 80326 participants in the Nurses' Health Study who had no history of cancer other than nonmelanoma skin cancer. Participants in the Nurses' Health Study reported on known and suspected ovarian cancer risk factors in questionnaires mailed biennially from 1976 to 1996. Food frequency questionnaires were included in the years 1980, 1984, 1986 and 1990. Newly reported ovarian cancer was documented by review of medical records. During 16 years of follow-up (1980-1996), 301 cases of invasive epithelial ovarian cancer were confirmed. Pooled logistic regression was used to control for age, body mass index (kg/m(2)), caffeine intake, oral contraceptive use, smoking history, parity and tubal ligation. For all subtypes of invasive ovarian cancer combined, we observed a nonsignificant 40% greater risk for women in the highest category of lactose consumption compared to the lowest (multivariate relative risk (RR) 1.40, 95% confidence interval (CI), 0.98-2.01). We observed a 2-fold higher risk of the serous ovarian cancer subtype among those in the highest category of lactose consumption compared to the lowest (RR 2.07, 95% CI, 1.27-3.40). For each 11-gram increase in lactose consumption (the approximate amount in one glass of milk), we observed a 20% increase in risk of serous cancers (RR 1.20, 95% CI, 1.04-1.39). Skim and low-fat milk were the largest contributors to dietary lactose. Women who consumed one or more servings of skim or low-fat milk daily had a 32% higher risk of any ovarian cancer (RR 1.32, 95% CI, 0.97-1.82) and a 69% higher risk of serous ovarian cancer (RR 1.69, 95% CI, 1.12-2.56) compared to women consuming 3 or less servings monthly. Controlling for fat intake did not change our findings. Our findings provide some support for the hypothesis that lactose intake increases risk of epithelial ovarian cancer. However, the observed excess risk appeared limited to the serous subtype of ovarian cancer in our study.

Adult↗

The transforming growth factor-beta1 (TGFB1) gene is associated with chronic obstructive pulmonary disease (COPD).

Although cigarette smoking is the primary environmental risk factor, genetic risk factors likely influence the development of chronic obstructive pulmonary disease (COPD). Linkage analysis between short-tandem repeat markers on chromosome 19 and COPD phenotypes was followed by association analysis of single nucleotide polymorphisms in a gene on chromosome 19q [transforming growth factor-beta1 (TGFB1)] and COPD phenotypes in a family-based sample and a case-control study (cases with severe COPD and control subjects with significant history of smoking but no COPD). Stratification by smoking status substantially improved the evidence of linkage to chromosome 19q for COPD phenotypes. Among former and current smokers in the Boston Early-Onset COPD Study, there was significant evidence of linkage between chromosome 19q and pre-bronchodilator (pre-BD) FEV(1) (LOD=3.30) and suggestive evidence of linkage between chromosome 19q and other COPD phenotypes. In these families, a SNP in the promoter region of TGFB1 (rs2241712) and two SNPs in the 3' genomic region of TGFB1 (rs2241718 and rs6957) were significantly associated with pre- and post-BD FEV(1) (P<0.05). Among smokers in the COPD cases and control subjects, two SNPs in the promoter region of TGFB1 (rs2241712 and rs1800469) and one SNP in exon 1 of TGFB1 (rs1982073) were significantly associated with COPD (P</=0.02 in all cases). Chromosome 19q likely contains a genetic locus (or loci) that influences COPD through an interaction with cigarette smoking. We hypothesize that genetic variants in or near the TGFB1 gene influence the pathogenesis of COPD among cigarette smokers.

Case-Control Studies↗

Lung cancer rates in men and women with comparable histories of smoking.

BACKGROUND: Recent case-control studies suggest that, given equal smoking exposure, women may have a higher relative risk of developing lung cancer than men. Despite prospective data that conflict with this hypothesis, mechanistic studies to find a biologic basis for a sex difference continue. METHODS: We addressed the hypothesis directly by analyzing prospective data from former and current smokers in two large cohorts--the Nurses' Health Study of women and the Health Professionals Follow-up Study of men. We calculated incidence rates and hazard ratios of lung cancer in women compared with men, adjusting for age, number of cigarettes smoked per day, age at start of smoking, and time since quitting, using Cox proportional hazards models. We also reviewed published results from prospective analyses. RESULTS: From 1986 through 2000, 955 and 311 primary lung cancers were identified among 60 296 women and 25 397 men, respectively, who ranged in age from 40 to 79 years. Incidence rates per 100 000 person-years for women and men were 253 and 232, respectively, among current smokers and 81 and 73, respectively, among former smokers. The hazard ratio in women ever smokers compared with men was 1.11 (95% confidence interval = 0.95 to 1.31). Six published prospective cohort studies allowed assessment of comparative susceptibility to lung cancer by sex. None supported an excess risk of lung cancer for women. CONCLUSIONS: Women do not appear to have a greater susceptibility to lung cancer than men, given equal smoking exposure. Research should be focused on enhancing preventive interventions for all.

Adult↗

A prospective study of sleep duration and mortality risk in women.

STUDY OBJECTIVES: It is commonly believed that 8 hours of sleep per night is optimal for good health. However, recent studies suggest the risk of death is lower in those sleeping 7 hours. We prospectively examined the association between sleep duration and mortality in women to better understand the effect of sleep duration on health. DESIGN: Prospective observational study. SETTING: Community-based. PARTICIPANTS: Women in the Nurses Health Study who answered a mailed questionnaire asking about sleep duration in 1986. INTERVENTIONS: None. MEASUREMENTS AND RESULTS: Vital status was ascertained through questionnaires, contact with next of kin, and the National Death Index. During the 14 years of this study (1986-2000), 5409 deaths occurred in the 82,969 women who responded to the initial questionnaire. Mortality risk was lowest among nurses reporting 7 hours of sleep per night. After adjusting for age, smoking, alcohol, exercise, depression, snoring, obesity, and history of cancer and cardiovascular disease, sleeping less than 6 hours or more than 7 hours remained associated with an increased risk of death. The relative mortality risk for sleeping 5 hours or less was 1.15 (95% confidence interval [CI], 1.02-1.29) for 6 hours, 1.01 (95% CI, 0.94-1.08), for 7 hours, 1.00 (reference group), for 8 hours, 1.12 (95% CI, 1.05-1.20), and for 9 or more hours 1.42 (95% CI, 1.27-1.58). CONCLUSIONS: These results confirm previous findings that mortality risk in women is lowest among those sleeping 6 to 7 hours. Further research is needed to understand the mechanisms by which short and long sleep times can affect health.

Adult↗

Alcohol intake and colorectal cancer: a pooled analysis of 8 cohort studies.

BACKGROUND: Epidemiologic studies have generally reported positive associations between alcohol consumption and risk for colorectal cancer. However, findings related to specific alcoholic beverages or different anatomic sites in the large bowel have been inconsistent. OBJECTIVE: To examine the relationship of total alcohol intake and intake from specific beverages to the incidence of colorectal cancer and to evaluate whether other potential risk factors modify the association. DESIGN: Pooled analysis of primary data from 8 cohort studies in 5 countries. SETTING: North America and Europe. PARTICIPANTS: 489,979 women and men with no history of cancer other than nonmelanoma skin cancer at baseline. MEASUREMENTS: Alcohol intake was assessed in each study at baseline by using a validated food-frequency questionnaire. RESULTS: During a maximum of 6 to 16 years of follow-up across the studies, 4687 cases of colorectal cancer were documented. In categorical analyses, increased risk for colorectal cancer was limited to persons with an alcohol intake of 30 g/d or greater (approximately > or =2 drinks/d), a consumption level reported by 4% of women and 13% of men. Compared with nondrinkers, the pooled multivariate relative risks were 1.16 (95% CI, 0.99 to 1.36) for persons who consumed 30 to less than 45 g/d and 1.41 (CI, 1.16 to 1.72) for those who consumed 45 g/d or greater. No significant heterogeneity by study or sex was observed. The association was evident for cancer of the proximal colon, distal colon, and rectum. No clear difference in relative risks was found among specific alcoholic beverages. LIMITATIONS: The study included only one measure of alcohol consumption at baseline and could not investigate lifetime alcohol consumption, alcohol consumption at younger ages, or changes in alcohol consumption during follow-up. It also could not examine drinking patterns or duration of alcohol use. CONCLUSIONS: A single determination of alcohol intake correlated with a modest relative elevation in colorectal cancer rate, mainly at the highest levels of alcohol intake.

Adult↗

Prospective study of postmenopausal hormone use and newly diagnosed asthma and chronic obstructive pulmonary disease.

BACKGROUND: Female reproductive hormones appear to influence asthma, although data are conflicting, and may modulate development of chronic obstructive pulmonary disease (COPD). Therefore, in a prospective cohort study, we evaluated whether postmenopausal hormone use was associated with an increased rate of newly diagnosed asthma and, separately, newly diagnosed COPD. METHODS: Postmenopausal hormone use was assessed by questionnaire biennially from 1976 onward. New physician diagnoses of asthma or COPD were reported on questionnaires from 1988 to 1996 and confirmed in 1998 using supplementary questionnaires. Grades of diagnostic certainty were established from reports of medication use and pulmonary function using validated definitions. RESULTS: During 546259 person-years of follow-up, current use of estrogen alone was associated with an increased rate of asthma (multivariate rate ratio, 2.29; 95% confidence interval [CI], 1.59-3.29) compared with those who never used hormones. Current users of estrogen plus progestin had a similarly increased rate of newly diagnosed asthma. Rate ratios increased with certainty of diagnosis of asthma. In contrast, rates of newly diagnosed COPD were the same among hormone users and nonusers (multivariate rate ratio, 1.05; 95% CI, 0.80-1.37). CONCLUSIONS: Postmenopausal hormone use was associated with an increased rate of newly diagnosed asthma but not newly diagnosed COPD. Female reproductive hormones may contribute to the onset of asthma among adult women, but do not appear to hasten the development of COPD.

Adult↗