Down's syndrome and maternal smoking in early pregnancy

Several previous studies have suggested that maternal smoking is associated with a decreased incidence of trisomy 21. By using the Swedish health registries, 1,321 infants with Down's syndrome (DS) were selected among 1,117,021 infants born in 1983–1993 with known smoking exposure in early pregnancy. No association between maternal smoking and all cases of DS was found [age-adjusted odds ratio (OR) for maternal smoking: 0.98; 95% confidence interval (CI): 0.86–1.11], but heterogeneity over strata existed. A slightly decreased OR (0.91; 95% CI: 0.72–1.15) for any maternal smoking was indicated among primiparas, but among multiparas, no effect of smoking on the incidence of DS could be detected (OR: 1.01; 95% CI: 0.87–1.17). The difference between the OR for smoking ≥10 cigarettes per day among primiparas (OR: 0.59; 95% CI: 0.38–0.90) and multiparas (OR: 1.06; 95% CI: 0.86–1.31) was statistically significant. If not due to statistical fluctuation, the findings indicate that no direct effect of smoking on DS risk exists but the association observed in primiparas is due to covarying factors. Genet. Epidemiol. 14:77–84,1997. © 1997 Wiley-Liss, Inc.     

Maternal reproductive history and the risk of isolated congenital malformations

We examined the relationship between maternal reproductive history and the newborn's risk of isolated congenital malformations in a large case-control cohort from the Polish Registry of Congenital Malformations. Congenital malformations were classified into four categories: isolated congenital heart defects (n=1673), isolated cleft palate (n=255), cleft lip with or without cleft palate (n=448) and renal agenesis (n=103). The case groups were compared with a shared group of 2068 controls recruited in the same time period and geographic area. Multivariable logistic regression was used to assess the risk associated with maternal gravidity and of previous miscarriages after accounting for maternal age and other potential risk factors. In unadjusted analyses, maternal gravidity was significantly associated with increased risk of all four classes of congenital malformations. After adjustment, a significant association persisted for congenital heart defects [odds ratio (OR)=1.22, [95% confidence interval (CI) 1.09, 1.36], P=0.0007] and cleft lip with or without cleft palate (OR=1.21, [95% CI 1.09, 1.36], P=0.0005). A similar trend existed for isolated cleft palate (OR=1.18, [95% CI 1.02, 1.37], P=0.03). There was no appreciable increase in the risk of congenital malformations associated with a maternal history of miscarriages, but a trend for a protective effect on the occurrence of cleft lip with or without cleft palate was observed (OR=0.72, [95% CI 0.52, 0.99], P=0.045). Based on our data, maternal gravidity represents a significant risk factor for congenital heart defects and cleft lip with or without cleft palate in the newborn infant. Our data do not support an increase in risk because of past history of miscarriages.     

Maternal smoking and congenital heart defects

The Swedish Child Cardiology Registry (CCR) and the Swedish Medical Birth Registry (MBR) were used to investigate a possible association between maternal smoking during pregnancy and congenital heart defects. Among 1,413,811 infants born in 1983–1996 with known smoking exposure in early pregnancy, 3384 infants with congenital heart defects were selected (458 term infants with persistent ductus arteriosus (PDA) identified from MBR or CCR, and 2926 infants with other heart defects, identified from CCR). After controlling for year of birth, maternal age, parity, and educational level, a weak, statistically significant association between all heart defects and maternal smoking was found (odds ratio (OR): 1.09; 95% confidence interval (CI): 1.01–1.19). When infants with isolated PDA were removed from the case group the significance disappeared (OR: 1.07; 95% CI: 0.98–1.17). For truncus abnormalities (OR: 1.23; 95% CI: 1.02–1.49), atrial septal defects (OR: 1.63; 95% CI: 1.04–2.57), and PDA (OR: 1.30; 95% CI: 1.05–1.62), a rather strong effect of maternal smoking was indicated. The increased OR for PDA remained when gestational duration and intrauterine growth was also controlled for. Further research based on independent data sets is needed to conclude whether the risk estimates for maternal smoking are true and truly differ between the groups. The classification system used (with 24 classes) is described in enough detail to permit a repetition of the study.     

Maternal cigarette smoking during pregnancy and risk of oral clefts in newborns.

The results of previous epidemiologic research on the possible association between maternal smoking during pregnancy and risk of oral clefts in offspring have been inconsistent. This may be due in part to methodological limitations, including imprecise measurement of tobacco use, failure to consider etiologic heterogeneity among types of oral clefts, and confounding. This analysis, based on a large case-control study, further evaluated the effect of first trimester maternal smoking on oral facial cleft risk by examining the dose-response relationship according to specific cleft type and according to whether or not additional malformations were present. A number of factors, including dietary and supplemental folate intake and family history of clefts, were evaluated as potential confounders and effect modifiers. Data on 3,774 mothers interviewed between 1976 and 1992 by the Slone Epidemiology Unit Birth Defects Study were used. Study subjects were actively ascertained from sites in areas around Boston, Massachusetts and Philadelphia, Pennsylvania; the state of Iowa; and southeastern Ontario, Canada. Cases were infants with isolated defects--cleft lip alone (n = 334), cleft lip and palate (n = 494), or cleft palate alone (n = 244)--and infants with clefts plus (+) additional malformations: cleft lip+ (n = 58), cleft lip and palate+ (n = 140), or cleft palate+ (n = 209). Controls were infants with defects other than clefts, excluding defects possibly associated with maternal cigarette use. There were no associations with maternal smoking for any oral cleft group, except for a positive dose response among infants with cleft lip and palate+ (for light smokers, odds ratio (OR) = 1.09 (95% confidence interval (CI): 0.6, 1.9); for moderate smokers, OR = 1.84 (95% CI: 1.2, 2.9); and for heavy smokers, OR = 1.85 (95% CI: 1.0, 3.5), relative to nonsmokers). This finding may be related to the additional malformations rather than to the cleft itself.     

Congenital malformations and maternal occupation: a registry based case-control study.

OBJECTIVES: To investigate the relations between congenital malformations and maternal occupation during pregnancy with a registry based case-control study. METHODS: Analysis was performed on data derived from the Florence Eurocat registry surveillance programme. The study included cases with isolated conditions, including chromosomal anomalies (n = 1351), cases with multiple anomalies registered during the 1980-91 period (n = 440), and babies with no congenital malformations recognised at birth who were born from 1982 to 1989 and selected as controls (n = 3223). 11 categories were defined, 10 including cases with isolated malformations and one for cases with multiple congenital anomalies. Four categories of maternal occupation were selected for the study. Odds ratio (OR) values were adjusted for maternal origin, maternal and paternal education, number of previous live births, illness during pregnancy, and maternal age when the group of chromosomal anomalies was analysed. RESULTS: A notable and significant association between oral clefts and mothers involved in leather and shoe manufacturing was found (adjusted OR 3.9; 99% confidence interval (99% CI) 1.5 to 9.8) and the risk consistently increased when considering cases with isolated cleft palate separately (OR 5.4; 95% CI 1.8 to 13.4). Moreover, a significant risk was identified for the association between multiple anomalies and textile dye workers (adjusted OR 1.9; 99% CI 1.0 to 3.8). CONCLUSIONS: This study indicates a notable, significant relation between maternal occupation as a pelt or leather worker and orofacial clefts in offspring. This finding is in agreement with the suggested inheritance models. The dilution effect due to studying large and heterogeneous groups of workers and occupations limits the value of the study; but it provides a good example of the use of a large database to search for teratogenic risk with the aid of malformation registries.     

Processed Meat and Colorectal Cancer Risk: A Pooled Analysis of Three Italian Case-Control Studies

To add evidence to the limited data available from southern Europe, we assessed the association between processed meat consumption and colorectal cancer risk. We analyzed data from three case-control studies conducted between 1985 and 2010 in various Italian areas, including a total of 3745 incident cases and 6804 hospital-based controls. We calculated odds ratios (ORs) and 95% confidence intervals (CIs) by unconditional multiple logistic regression models. The median consumption of processed meat was around 20 g/day both in cases and controls. The OR of colorectal cancer was 1.02 (95% CI 0.99–1.04) for an increase of 10 g/day of processed meat. The association was statistically significant for colon cancer (OR 1.03, 95% CI 1.00–1.06), particularly for proximal colon cancer (OR 1.09, 95% CI 1.04–1.14), while there was no relation with rectal cancer (OR 0.99, 95% CI 0.95–1.03). The OR of proximal colon cancer was 1.38 (95% CI 1.08–1.75) for the highest sex-specific tertile of consumption (>25 g/day for men, >21.5 for women) compared with the lowest (<15 g/day), whereas no significant ORs were found for other anatomical subsites. Our findings indicate that there is no association with colorectal cancer overall, in the presence, however, of a positive association with proximal colon cancer.     

Maternal occupation in the leather industry and selected congenital malformations

OBJECTIVES: Data from a hospital based case-control study were analysed to assess the relation between maternal occupation in the leather industry and several groups of congenital defects (nervous system, cardiac defects of closure, oral cleft, epispadia or hypospadia, and multiple anomalies). METHODS: Cases and controls were selected from eight public hospitals in Comunidad Valenciana, Spain, in 1993 and 1994. Cases were located from the hospital discharge records, including children born and diagnosed in some of the selected hospitals during their first year of life. Controls were selected from births without congenital defects in the same hospitals and dates of the cases (ratio 1:1). Both parents of selected children were interviewed (mainly by phone) and information about potential confounding variables and occupational history during the three years before the birth was collected in structured questionnaires. RESULTS: A total of 261 cases and the same number of controls were included in the study. Adjusted odds ratios (ORs) were estimated for maternal occupation in the leather industry in the period between three months before the conception and the birth of the child (n = 22), and each selected group of congenital malformations: nervous system defects (OR 1.02, 95% confidence interval (95% CI) 0.12 to 8.51), cardiac defects of closure (OR 1.78, 95% CI 0.44 to 7.17), oral clefts (OR 6.18, 95% CI 1.48 to 25.69), for epispadia or hypospadia (OR 4.05, 95% CI 0.77 to 21.44), and multiple anomalies (OR 3.14, 95% CI 0.82 to 12.00). CONCLUSION: These data are compatible with an increased risk for oral clefts in the offspring of women working in the leather industry. Some other categories of defect could have an increased risk as well, although for these our data cannot exclude random error as an explanation. Given these results and previous findings in similar studies, some precautionary recommendations regarding maternal exposure in leather industries, probably in relation to solvents, would be justified.

 

     

孕妇被动吸烟与低出生体重关系的Meta分析

目的分析孕妇孕早期和不同孕期被动吸烟对新生儿低出生体重的影响。方法通过Meta分析方法分析孕妇被动吸烟与新生儿低出生体重之间的关系。对NCBI、OVID-MEDLINE、CNKI、VIP以及CBM数据库进行检索(截止日期为2008年4月),结果报告合并OR值及95%CI。结果共获得26篇文献,其中队列研究20篇,病例对照研究6篇。总体分析,孕妇被动吸烟的合并效应值OR=1.65(95%CI:1.39～1.97);调整合并效应值OR=1.60(95%CI:1.25～2.05);最低和最高暴露量的合并效应值分别为OR=1.53(95%CI:1.14～2.04)和OR=2.53(95%CI:1.46～4.36);孕早期暴露的合并效应值OR=1.12(95%CI:0.82～1.55),没有统计学意义。结论孕妇被动吸烟增加新生儿低出生体重的危险性;孕中晚期可能是被动吸烟效应的敏感期;被动吸烟的阈值是否存在尚不明确。     

A case-control study of maternal smoking and congenital malformations

We conducted a population-based case-control study to assess the association between maternal smoking during pregnancy and the risk of giving birth to a child with a congenital malformation. Cases were all singleton livebirths with a congenital malformation recorded on the 1984-1986 Washington State Birth Records (n = 3284). The smoking histories of these mothers were compared to a randomly selected group of mothers with a singleton livebirth of a child without a malformation during these same years (n = 4500). When all malformations were taken as a group, there was no association with maternal smoking (relative risk (RR) = 1.0, 95% CI 0.9-1.1). However, increased risks were observed for a number of specific malformations, including microcephalus (RR = 2.0, 95% CI 1.0-4.0), cleft defects (RR = 1.4, 95% CI 1.0-2.0), and club foot (RR = 1.4, 95% CI 1.0-2.0). We did not find any association with Down's syndrome (RR = 0.8 95% CI 0.5-1.3) or any other malformation. We conclude that maternal smoking during pregnancy may be associated with an increased risk for some malformations.     

Maternal ethnicity and pre-eclampsia in New York City, 1995-2003

Studies on ethnic differences in the risk of pre-eclampsia are limited. We linked birth records for 902,460 singleton births for the period 1995-2003 in New York City with hospital discharge data to evaluate the association between ethnicity and the risk of pre-eclampsia and compare risks between US-born and foreign-born women. Logistic regression models adjusted for maternal age, maternal education, parity, self-reported pre-pregnancy maternal weight, smoking during pregnancy and year of delivery were used to compare each ethnic group with non-Hispanic White women. The prevalence of pre-eclampsia in this study population was 3.2%. Among the major ethnic groups considered in our study, East Asian women had the lowest risk of pre-eclampsia (1.4%) and Mexican women had the highest risk (5.0%). Compared with non-Hispanic White women, there was a slightly decreased risk for East Asian women (adjusted OR = 0.8, [95% CI 0.7, 0.8]), similar risk for North African women (adjusted OR = 1.1, [95% CI 0.9, 1.3]), and increased risk for all other major ethnic groups (adjusted ORs: 1.3, 2.9), with the highest risk for Mexican women (adjusted OR = 2.9, [95% CI 2.7, 3.1]). No difference in risks was observed for US- vs. foreign-born women with the exception that foreign-born South-East Asian and Pacific Islanders had an increased risk of pre-eclampsia (adjusted OR = 1.8, [95% CI 1.0, 3.1]) relative to those born in the US. We concluded that there was ethnic heterogeneity in the development of pre-eclampsia among women in New York City and that Asian subgroups should be examined separately in future studies on ethnicity. Our results should contribute to screening for pre-eclampsia taking ethnic variation into account, and may help to suggest leads for the study of the aetiology of the condition.     

A case-control study of maternal smoking and congenital malformations

Summary. We conducted a population-based case-control study to assess the association between maternal smoking during pregnancy and the risk of giving birth to a child with a congenital malformation. Cases were all singleton livebirths with a congenital malformation recorded on the 1984–1986 Washington State Birth Records (n = 3284). The smoking histories of these mothers were compared to a randomly selected group of mothers with a singleton livebirth of a child without a malformation during these same years (n = 4500). When all malformations were taken as a group, there was no association with maternal smoking (relative risk (RR) = l.0, 95% CI 0.9–1.1). However, increased risks were observed for a number of specific malformations, including microcephalus (RR = 2.0, 95% CI 1.0–4.0), cleft defects (RR=1.4, 95% CI 1.0–2.0), and club foot (RR= 1.4, 95% CI 1.0–2.0). We did not find any association with Down's syndrome (RR=0.8, 95% CI 0.5–1.3) or any other malformation. We conclude that maternal smoking during pregnancy may be associated with an increased risk for some malformations.     

Maternal Smoking, Breastfeeding, and Risk of Childhood Overweight: Findings from a National Cohort

To examine the association between exposure to tobacco compounds in breast milk and risk of childhood overweight, we used historical data for a subset of 21,063 mother–child pairs in the US Collaborative Perinatal Project. Based on self-reports, mothers were classified as non-smokers, light (1–9 cigarettes/day), moderate (10–19), or heavy (20+) smokers. Feeding type (exclusive breastfeeding or bottle-feeding) was observed during nursery stay after birth. We stratified children by maternal smoking and feeding type, and then fit interaction terms to isolate exposure to tobacco compounds via breast milk from exposure in uterus and in ambient air after birth. Using measured weight and height, overweight at age 7 was defined as a body mass index ≥85th percentile by sex and age. Among exclusively bottle-fed children, adjusted odds ratios (ORs) of overweight at age 7 were 1.24 (95 % confidence interval [CI], 1.12–1.38; vs. non-smoking) for light maternal smoking, 1.43 (95 % CI, 1.25–1.63) for moderate maternal smoking, and 1.46 (95 % CI, 1.28–1.66) for heavy maternal smoking. Among exclusively breastfed children, the corresponding ORs were 1.33 (95 % CI, 0.96–1.84) for light, 1.86 (95 % CI, 1.27–2.73) for moderate, and 2.22 (95 % CI, 1.53–3.20) for heavy maternal smoking. There was a modest positive interaction between breastfeeding and heavy maternal smoking on overweight risk at age 7. Tobacco compounds via breast milk of smoking mothers (significantly for heavy smokers) appear to be associated with a modest elevation in childhood overweight risk at 7 years of age. More aggressive intervention is needed to help pregnant and breastfeeding women to quit smoking.     

Perinatal risk factors for infantile autism

BACKGROUND: Etiologic hypotheses in infantile autism suggest a strong genetic component, as well as possible environmental risks linked to early fetal development. We evaluated the association of maternal, pregnancy, delivery, and infant characteristics and risk of infantile autism. METHODS: We conducted a case-control study nested within a population-based cohort (all Swedish children born in 1974-1993). We used prospectively recorded data from the Swedish Birth Register, which were individually linked to the Swedish Inpatient Register. Cases were 408 children (321 boys and 87 girls) discharged with a main diagnosis of infantile autism from any hospital in Sweden before 10 years of age in the period 1987-1994, plus 2,040 matched controls. Conditional logistic regression was used to calculate odds ratios (ORs) and 95% confidence intervals (CIs). RESULTS: The risk of autism was associated with daily smoking in early pregnancy (OR = 1.4; CI = 1.1-1.8), maternal birth outside Europe and North America (OR = 3.0; CI = 1.7-5.2), cesarean delivery (OR = 1.6; CI = 1.1-2.3), being small for gestational age (SGA; OR = 2.1; CI = 1.1-3.9), a 5-minute Apgar score below 7 (OR = 3.2, CI = 1.2-8.2), and congenital malformations (OR = 1.8, CI = 1.1-3.1). No association was found between autism and head circumference, maternal diabetes, being a twin, or season of birth. CONCLUSIONS: Our findings suggest that intrauterine and neonatal factors related to deviant intrauterine growth or fetal distress are important in the pathogenesis of autism.     

Using case-control designs for genome-wide screening for associations between genetic markers and disease susceptibility loci

We used a case-control design to scan the genome for any associations between genetic markers and disease susceptibility loci using the first two replicates of the Mycenaean population from the GAW11 (Problem 2) data. Using a case-control approach, we constructed a series of 2-by-3 tables for each allele of every marker on all six chromosomes. Odds ratios (ORs) and 95% confidence intervals (95% CI) were estimated for all alleles of every marker. We selected the one allele for which the estimated OR had the minimum p-value to plot in the graph. Among these selected ORs, we calculated 95% CI for those that had a p-value < or = adjusted alpha level. Significantly high ORs were taken to indicate an association between a marker locus and a suspected disease-susceptibility gene. For the Mycenaean population, the case-control design identified allele number 1 of marker 24 on chromosome 1 to be associated with a disease susceptibility gene, OR = 2.10 (95% CI 1.66-2.62). Our approach failed to show any other significant association between case-control status and genetic markers. Stratified analysis on the environmental risk factor (E1) provided no further evidence of significant association other than allele 1 of marker 24 on chromosome 1. These data indicate the absence of linkage disequilibrium for markers flanking loci A, B, and C. Finally, we examined the effect of gene x environment (G x E) interaction for the identified allele. Our results provided no evidence of G x E interaction, but suggested that the environmental exposure alone was a risk factor for the disease.     

Persistent chlorinated pesticides and intra-uterine foetal growth retardation: a possible association

OBJECTIVE: To examine the association between DDT (dichlorodiphenyl trichloroethane) and HCH (hexachlorocyclohexane) exposure and intra-uterine growth retardation (IUGR, <10th percentile of birth weight for gestational age). METHOD: We detected p,p'-DDT, o,p'-DDT, p,p'-DDD, p,p'-DDE and alpha-HCH, beta-HCH, gamma-HCH, delta-HCH in maternal blood, placenta and cord blood, collected at parturition, from mothers with IUGR babies ( n=30) and from those with babies of normal weight ( n=24), using gas-liquid chromatography equipped with electron capture detector ((63)Ni). The adjusted odds ratios (ORs) for these pesticides in mothers and infants were determined by multiple logistic regression. RESULTS: There were statistically significant associations ( P<0.05) between maternal blood levels of alpha-HCH (OR=1.22; 95% CI: 1.02-1.46), gamma-HCH (OR=1.38; 95%CI: 1.05-1.80), delta-HCH (OR=1.61; 95% CI: 1.01-2.54), total HCH (OR=1.07; 95% CI: 1.01-1.13) and p,p'-DDE (OR=1.21; 95%CI:1.03-1.42) and IUGR after adjustment for potential confounders. Also, significant association (P<0.05) between cord blood levels of gamma-HCH (OR=1.14; 95% CI: 1.00-1.31), delta-HCH (OR=1.31; 95% CI: 1.00-1.75), total HCH (OR=1.07; 95% CI: 1.00-1.14) and IUGR were found after adjustment for potential confounders. A significant negative correlation between body weight of newborn babies and p,p'-DDE in maternal blood (r= -0.25; P<0.05) and delta-HCH and p,p'-DDE in the cord blood (r= -0.27 and -0.26; P<0.05) was noticed after gestational age had been accounted for. CONCLUSION: Exposure of pregnant women to organochlorine pesticides may increase the risk of IUGR, which is a contributing factor for infant mortality in India.     

Association between adult height, genetic susceptibility and risk of glioma

BACKGROUND: Some, but not all, observational studies have suggested that taller stature is associated with a significant increased risk of glioma. In a pooled analysis of observational studies, we investigated the strength and consistency of this association, overall and for major sub-types, and investigated effect modification by genetic susceptibility to the disease. METHODS: We standardized and combined individual-level data on 1354 cases and 4734 control subjects from 13 prospective and 2 case-control studies. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) for glioma and glioma sub-types were estimated using logistic regression models stratified by sex and adjusted for birth cohort and study. Pooled ORs were additionally estimated after stratifying the models according to seven recently identified glioma-related genetic variants. RESULTS: Among men, we found a positive association between height and glioma risk (≥190 vs 170-174 cm, pooled OR = 1.70, 95% CI: 1.11-2.61; P-trend = 0.01), which was slightly stronger after restricting to cases with glioblastoma (pooled OR = 1.99, 95% CI: 1.17-3.38; P-trend = 0.02). Among women, these associations were less clear (≥175 vs 160-164 cm, pooled OR for glioma = 1.06, 95% CI: 0.70-1.62; P-trend = 0.22; pooled OR for glioblastoma = 1.36, 95% CI: 0.77-2.39; P-trend = 0.04). In general, we did not observe evidence of effect modification by glioma-related genotypes on the association between height and glioma risk. CONCLUSION: An association of taller adult stature with glioma, particularly for men and stronger for glioblastoma, should be investigated further to clarify the role of environmental and genetic determinants of height in the etiology of this disease.     

Early intrauterine exposure to tobacco-inhaled products and obesity

An association between maternal smoking during pregnancy and offspring obesity has been reported. This study assessed the impact of maternal smoking during the first trimester. Data on 4,974 German children aged 5-6 years were obtained at school entry health examinations in 2001-2002 in Bavaria. Obesity was defined by body mass index using International Obesity Task Force cutpoints. Prevalence of obesity was 1.9% (95% confidence interval (CI): 1.5, 2.4) in offspring of never smokers, 4.5% (95% CI: 2.9, 6.7) for maternal smoking during the first trimester only, and 5.9% (95% CI: 3.8, 8.7) for maternal smoking throughout pregnancy. Unadjusted odds ratios were higher for maternal smoking throughout pregnancy (odds ratio = 3.23, 95% CI: 2.00, 5.21) compared with the first trimester only (odds ratio = 2.41, 95% CI: 1.49, 3.91). Adjusted odds ratios were similar: 1.70 (95% CI: 1.02, 2.87) for maternal smoking throughout pregnancy and 2.22 (95% CI: 1.33, 3.69) for maternal smoking in the first trimester only. When modeled together, no statistically significant difference in obesity risk was found between maternal smoking in the first trimester compared with throughout pregnancy. The effect of intrauterine tobacco exposure on childhood obesity may depend largely on cigarette smoking during the first trimester, whereas the additional impact of smoking throughout pregnancy might be due to confounding by sociodemographics. Women should be encouraged to quit smoking prior to conception.     

中国人群吸烟与喉癌关系的Meta分析

目的综合评价中国人群吸烟与喉癌之间的关系及关联强度,为我国喉癌的防治策略提供依据。方法在CNKI、万方、维普、PubMed、ScienceDirect、SpringerLink、Wiley、ProQuest等数据库中系统检索截止2013年1月之前国内外发表的相关研究文献。所有文献检索、文献选取、文献信息的提取及文献质量评价均由两人独立进行。根据研究之间的异质性大小采用合适的方法来合并相关结果。结果纳入合格研究文献16篇,喉癌患者2730例,对照3224例。吸烟与喉癌发病关系的合并0尺值为4．08（95％CI：2．90—5．26;r=86．7％,P〈0．001）。很少吸烟者及经常吸烟者发生喉癌的OR值为分别为5．90（95％CI：3．05～11．41）及13．30（95％CI：8．03～22．03）。结合漏斗图的结果,尚不能认为目前纳入的研究存在发表偏倚（Egger,P=0．402;Begg,P=0．784）。结论在中国,吸烟会显著增加喉癌的发病风险,而且随着吸烟量的增加,喉癌的风险可能更高。     

Spontaneous abortion and maternal work in greenhouses

BACKGROUND: A positive association between maternal occupational exposure to pesticide and spontaneous abortion has been reported in some studies. Work in greenhouses may imply exposure of pregnant women to pesticides continuously and at elevated level. METHODS: A total of 717 women working in greenhouses provided information on 973 pregnancies, including 110 spontaneous abortions. These pregnancies were classified as exposed or not exposed according to maternal occupation, re-entry activities and application of pesticides in greenhouses during at least 1 month in the first trimester of pregnancy. The ORs for spontaneous abortion were estimated through a generalised estimate equations model for all orders of pregnancy together, and through a logistic regression model limited to first pregnancies. RESULTS: Increased risks of spontaneous abortion were found for maternal re-entry activities within 24 hr after pesticides were applied (all orders of pregnancy: OR 3.2, 95% CI 1.3-7.7; first pregnancies: OR 3.8, 95% CI 1.0-13.9) and for those who applied pesticides (all orders of pregnancy: OR 2.6, 95% CI 1.0-6.6; first pregnancies: OR 3.7, 95% CI 0.7-20,6) CONCLUSIONS: The observed results support the hypothesis of an association between maternal work in greenhouses and spontaneous abortion. The main limitations of the study are lack of information on the specific chemicals used and the small number of pregnancies heavily exposed to pesticides.     

Association between maternal occupational exposure to organic solvents and congenital heart defects, National Birth Defects Prevention Study, 1997-2002

Objective To examine the relation between congenital heart defects (CHDs) in offspring and estimated maternal occupational exposure to chlorinated solvents, aromatic solvents and Stoddard solvent during the period from 1 month before conception through the first trimester. Methods The study population included mothers of infants with simple isolated CHDs and mothers of control infants who delivered from 1997 through 2002 and participated in the National Birth Defects Prevention Study. Two methods to assess occupational solvent exposure were employed: an expert consensus-based approach and a literature-based approach. Multiple logistic regression was used to calculate adjusted ORs and 95% CIs for the association between solvent classes and CHDs. Results 2951 control mothers and 2047 CHD case mothers were included. Using the consensus-based approach, associations were observed for exposure to any solvent and any chlorinated solvent with perimembranous ventricular septal defects (OR 1.6, 95% CI 1.0 to 2.6 and OR 1.7, 95% CI 1.0 to 2.8, respectively). Using the literature-based approach, associations were observed for: any solvent exposure with aortic stenosis (OR 2.1, 95% CI 1.1 to 4.1) and Stoddard solvent exposure with d-transposition of the great arteries (OR 2.0, 95% CI 1.0 to 4.2), right ventricular outflow tract obstruction defects (OR 1.9, 95% CI 1.1 to 3.3) and pulmonary valve stenosis (OR 2.1, 95% CI 1.1 to 3.8). Conclusions The authors found evidence of associations between occupational exposure to solvents and several types of CHDs. These results should be interpreted in light of the potential for misclassification of exposure.