Age at first childbirth and later poverty.
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Asian Indians from the Indian subcontinent have low rates of breast cancer, but studies on breast cancer risk factors in Indian and Pakistani women living in the United States are lacking. This study contrasted breast cancer risk factors [serum total 17 beta-estradiol (E2), sex hormone-binding globulin-bound E2, available E2, estrone (E1), and dehydroepiandrosterone sulfate, reproductive history, family history of cancer, body composition/size, dietary intake, physical activity, and excretion of isoflavones] between two distinct ethnic groups of premenopausal women residing in the United States. We also determined the contribution of these and other factors to the variability of each sex hormone. Distributions of values for serum total E2, available E2, and sex hormone-binding globulin-bound E2 (%) were greater (p < 0.005) in American (n = 47) than in Indian and Pakistani (n = 47) women. Multiple regression analysis indicated that 26% of the variability (p < or = 0.0001) in serum E2 was accounted for by the ratio of total cholesterol to high-density-lipoprotein cholesterol, length of time in the United States, and saturated fat intake, whereas less (17%) variability was accounted for by available E2 (representing free E2 + albumin-bound E2), contributed by the ratio of total cholesterol to high-density-lipoprotein cholesterol and saturated fat intake. Five variables accounted for 31% of the variability (p < or = 0.0001) in E1. The major finding of this study was that circulating sex hormone concentrations were determined more by environmental factors than by ethnicity, which was not a significant contributor to any of the serum hormones.
Benign breast disease (BBD) is common in women in the reproductive age group. The results of epidemiological studies that have examined the relationship between diet and BBD are controversial and scarce. The aim of the present study was to identify and evaluate the impact of dietary and reproductive risk factors in the development of BBD in Mexican women. Between 1994 and 1996, 121 women with BBD and 121 age-matched (+/- 3 yr) clinical controls with non-breast-related diseases were identified. The study population was directly interviewed about their reproductive history, and a semiquantitative food frequency questionnaire was used to obtain dietary information. The population was originally identified as part of a hospital-based case-control study examining exposure to 1,1-bis(p-chlorophenyl)-2,2,2-trichloroethane and breast cancer. A significant reduction in the risk of BBD was observed when comparing the upper with the lower tertiles of consumption of citrus fruit [odds ratio (OR) = 0.43, 95% confidence interval (CI) = 0.21-0.88], non-citrus fruit (OR = 0.35, 95% CI = 0.16-0.76), diary products (OR = 0.36, 95% CI = 0.18-0.75), and food sources of lignans (OR = 0.48, 95% CI = 0.24-0.98). A marginally significant reduction in the risk of BBD associated with the consumption of vitamin B-12 (OR = 0.48, 95% CI = 0.23-1.02) was also observed. Our results add new information about the role of diet in the etiology of BBD.
Fetal cells circulate in pregnant women and persist in blood and tissue for decades post-partum. The mother thus becomes chimeric. Factors that may influence such fetal cell microchimerism include histocompatibility, fetal or placental abnormalities, or a reproductive history that includes miscarriage or elective termination. Fetal cell microchimerism is associated with some maternal autoimmune diseases, such as systemic sclerosis. Moreover, a novel population of fetal cells, the pregnancy-associated progenitor cells (PAPCs), appears to differentiate in diseased or injured maternal tissue. The cellular origin of these cells is at present unknown but could be a hematopoietic stem cell, a mesenchymal stem cell, or a novel cell type. Pregnancy therefore results in the acquisition of cells with stem-cell-like properties that may influence maternal health post-partum. Rather than triggering disease, these cells may instead combat it.
The study was aimed at investigating the conditions and circumstances for the recruitment of prostitutes, as well as their reproductive history, working conditions, knowledge of and attitudes to sexually transmitted diseases (STDs), and use of prophylactic antibiotic therapy of these diseases. Two hundred prostitutes were investigated by in-depth interviews at STD clinics, private practices and hotels. Of the 200 prostitutes, 8 (4%) were less than 15 years old and 32 (16%) more than 25 years old. Most of the women came from rural villages. Half of them were gypsies. Most had a boyfriend (often the pimp). One-quarter had been or were on their way abroad to prostitute. Half were migrating within Bulgaria to prostitute. They claimed a high rate of condom use with customers, but seldom with their pimps or boyfriends. About one-tenth used antibiotics prophylactically. They had knowledge of classical STDs and HIV/AIDS but only in exceptional cases had they heard about chlamydial and human papillomavirus infections. They often cohabited with a female friend also often practising prostitution. It was concluded that recruitment is often easy as the prostitute can earn more from only one contact with a customer than their parents earn from work in a month. Symptoms suggestive of STD were very common in the prostitutes, i.e. in 43%. Bulgaria is a recruitment area for international prostitutes.
There is conflicting research regarding an association between fetal death and paternal exposure to Agent Orange, a phenoxy herbicide widely used in Vietnam that was contaminated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Men who worked in the U.S. factories that produced Agent Orange were exposed to TCDD at levels hundreds of times higher than TCDD levels in the general population. Wives of TCDD-exposed chemical workers and wives of nonexposed neighborhood referents were interviewed to determine reproductive history. Paternal serum TCDD level at time of conception was estimated for each pregnancy using serum samples taken in 1987. Estimated TCDD levels of workers during or after exposure were high (median, 254 ppt; range, 3-16,340 ppt) compared to referent levels (median, 6 ppt; range, 2-19 ppt). No association between paternal TCDD level at the time of conception and spontaneous abortion was observed among pregnancies fathered by workers with TCDD levels of < 20 ppt [odds ratio (OR) = 0.77; 95% confidence interval (CI), 0.48-1.22], 20 to < 255 ppt (OR = 0.81; 95% CI, 0.40-1.63), 255 to < 1,120, (OR = 0.69; 95% CI, 0.30-1.58), and >or= 1,120 ppt (OR = 0.95; 95% CI, 0.42-2.17) compared to pregnancies fathered by referents. The sex ratio [males/(males + females)] of offspring also did not differ by TCDD exposure (0.53 and 0.54 among workers and referents, respectively). We did not find an association between paternal serum TCDD level and spontaneous abortion or sex ratio of offspring in this population. The estimated TCDD levels in this exposed worker population were much higher than in other studies, providing additional evidence that paternal TCDD exposure does not increase the risk of spontaneous abortion at levels above those observed in the general population. The study could not evaluate the effect of father's childhood or prenatal TCDD exposure on subsequent sex ratio.
Exposures to ambient air pollutants have been associated with adverse birth outcomes. We investigated the effects of air pollutants on birth weight mediated by reduced fetal growth among term infants who were born in California during 1975-1987 and who participated in the Children's Health Study. Birth certificates provided maternal reproductive history and residence location at birth. Sociodemographic factors and maternal smoking during pregnancy were collected by questionnaire. Monthly average air pollutant levels were interpolated from monitors to the ZIP code of maternal residence at childbirth. Results from linear mixed-effects regression models showed that a 12-ppb increase in 24-hr ozone averaged over the entire pregnancy was associated with 47.2 g lower birth weight [95% confidence interval (CI), 27.4-67.0 g], and this association was most robust for exposures during the second and third trimesters. A 1.4-ppm difference in first-trimester carbon monoxide exposure was associated with 21.7 g lower birth weight (95% CI, 1.1-42.3 g) and 20% increased risk of intrauterine growth retardation (95% CI, 1.0-1.4). First-trimester CO and third-trimester O3 exposures were associated with 20% increased risk of intrauterine growth retardation. A 20-microg/m3 difference in levels of particulate matter < or = 10 microm in aerodynamic diameter (PM10) during the third trimester was associated with a 21.7-g lower birth weight (95% CI, 1.1-42.2 g), but this association was reduced and not significant after adjusting for O3. In summary, O3 exposure during the second and third trimesters and CO exposure during the first trimester were associated with reduced birth weight.
The first step in modeling lead kinetics during pregnancy includes a description of sequential maternal blood lead (PbB) during pregnancy and the factors controlling it. We analyzed PbB of 105 women living in the Valley of Mexico from week 12 to week 36 of pregnancy and again at parturition. We also used data from all women contributing blood at any stage of pregnancy to determine antecedents of PbB. Pregnancies were uneventful, and offspring were normal. Although geometric mean PbB level averaged around 7.0 micrograms/dl (0.34 mumol/l), with a range of 1.0-35.5 micrograms/dl throughout pregnancy, analysis of variance revealed a significant decrease in mean PbB from week 12 to week 20 (1.1 micrograms/dl) and various significant increases in mean PbB from week 20 to parturition (1.6 micrograms/dl). Regression analyses confirmed the positive linear PbB trend from 20 weeks to parturition and additional contributions of dietary calcium, reproductive history, lifetime residence of Mexico City, coffee drinking, and use of indigenous lead-glazed pottery. Although decreasing hematocrit has been suggested to explain first-half pregnancy PbB decrease, the time course of hematocrit decrease in the present study did not match the sequential changes in PbB. While hemodilution and organ growth in the first half of pregnancy may account for much of the PbB decrease seen between 12 and 20 weeks, the remaining hemodilution and accelerated organ growth of the last half of pregnancy do not predict the trend toward increasing maternal PbB concentration from 20 weeks to delivery. Mobilization of bone lead, increased gut absorption, and increased retention of lead may explain part of the upward PbB trend in the second half of pregnancy. Reduction of lifetime lead exposure may be required to decrease risk of fetal exposure.
Breast cancer, the most frequent spontaneous malignancy diagnosed in women in the western world, is continuously increasing in incidence in industrialized nations. Although breast cancer develops in women as the result of a combination of external and endogenous factors such as exposure to ionizing radiation, diet, socioeconomic status, and endocrinologic, familial, or genetic factors, no specific etiologic agent(s) or the mechanisms responsible of the disease has been identified as yet. Thus, experimental models that exhibit the same complex interactions are needed for testing various mechanisms and for assessing the carcinogenic potential of given chemicals. Rodent mammary carcinomas represent such a model to a great extent because, in these species, mammary cancer is a multistep complex process that can be induced by either chemicals, radiation, viruses, or genetic factors. Long-term studies in rodent models have been particularly useful for dissecting the initiation, promotion, and progression steps of carcinogenesis. The susceptibility of the rodent mammary gland to develop neoplasms has made this organ a unique target for testing the carcinogenic potential of specific genotoxic chemicals and environmental agents. Mammary tumors induced by indirect- or direct-acting carcinogens such as 7, 12-dimethlbenz(a)anthracene or N-methyl-N-nitrosourea are, in general, hormone dependent adenocarcinomas whose incidence, number of tumors per animal, tumor latency, and tumor type are influenced by the age, reproductive history, and endocarinologic milieu of the host at the time of carcinogen exposure. Rodent models are informative in the absence of human data. They have provided valuable information on the dose and route of administration to be used and optimal host conditions for eliciting maximal tumorigenic response. Studies of the influence of normal gland development on the pathogenesis of chemically induced mammary carcinomas have clarified the role of differentiation in cancer initiation. Comparative studies with the development of the human breast and the pathogenesis of breast cancer have contributed to validate rodent-to-human extrapolations. However, it has not been definitively established what type of information is necessary for human risk assessment, whether currently toxicity testing methodologies are sufficient for fulfilling those needs, or whether treatment-induced tumorigenic responses in rodents are predictive of potential human risk. An alternative to the traditional bioassays are mechanism-based toxicology and molecular and cellular approaches, combined with comparative in vitro systems. These approaches might allow the rapid screen of chemicals for setting priorities for further studies to determine the dose-response relationship for chemical effects at low doses, to assess effects other than mutagenesis and/or tumorigenesis, or to establish qualitative and quantitative relationships of biomarkers to toxic effects. Until there is enough information on the predictive value of mechanism-based toxicology for risk assessment, this approach should be used in conjunction with and validated by the traditional in vivo long-term bioassays.
Prior studies reported an association between ambient air concentrations of total suspended particles and SO2 during pregnancy and adverse pregnancy outcomes. We examined the possible impact of particulate matter up to 10 microm (PM10) and up to 2.5 microm (PM2. 5) in size on intrauterine growth retardation (IUGR) risk in a highly polluted area of Northern Bohemia (Teplice District). The study group includes all singleton full-term births of European origin over a 2-year period in the Teplice District. Information on reproductive history, health, and lifestyle was obtained from maternal questionnaires. The mean concentrations of pollutants for each month of gestation were calculated using continuous monitoring data. Three intervals (low, medium, and high) were constructed for each pollutant (tertiles). Odds ratios (ORs) for IUGR for PM10 and PM2.5 levels were generated using logistic regression for each month of gestation after adjustment for potential confounding factors. Adjusted ORs for IUGR related to ambient PM10 levels in the first gestational month increased along the concentration intervals: medium 1.62 [95% confidence interval (CI), 1.07-2.46], high 2.64 (CI, 1.48-4.71). ORs for PM2.5 were 1.26 (CI, 0.81-1.95) and 2.11 (CI, 1. 20-3.70), respectively. No other associations of IUGR risk with particulate matter were found. Influence of particles or other associated air pollutants on fetal growth in early gestation is one of several possible explanations of these results. Timing of this effect is compatible with a current hypothesis of IUGR pathogenesis. Seasonal factors, one of the other possible explanations, is less probable. More investigation is required to examine these findings and alternative explanations.
The purpose of this study was to review published studies on the variability of age at menarche and age at menopause throughout the world, and to identify the main causes for age variation in the timing of these events. We first present a summary table including mean (or median) values of the age at menarche in 67 countries, and of the age at menopause in 26 countries. General linear models showed that mean age at menarche was strongly linked to the mean female life expectancy, suggesting that one or several variables responsible for inequalities in longevity similarly influenced the onset of menarche. A closer examination of the data revealed that among several variables reflecting living conditions, the factors best explaining the variation in age at menarche were adult illiteracy rate and vegetable calorie consumption. Because adult illiteracy rate has some correlation with the age at which children are involved in physical activities that can be detrimental in terms of energy expenditure, our results suggest that age at menarche reflects more a trend in energy balance than merely nutritional status. In addition, we found the main determinant of age at menopause to be the mean fertility. This study thus suggests that, on a large scale, age at menarche is mainly determined by extrinsic factors such as living conditions, while age at menopause seems to be mainly influenced by intrinsic factors such as the reproductive history of individuals. Finally, these findings suggest that human patterns cannot be addressed solely by traditional, small-scale investigations on single populations. Rather, complementary research on a larger scale, such as this study, may be more appropriate in defining some interesting applications to the practical problems of human ecology.
Eighty-nine canine mammary tumors and dysplasias of 66 bitches were investigated to determine the immunohistochemical expression of classical estrogen receptor (ER-alpha) and its clinical and pathologic associations and prognostic value. A complete clinical examination was performed and reproductive history was evaluated. After surgery, all animals were followed-up for 18 months, with clinical examinations every 3-4 months. ER-alpha expression was higher in tumors of genitally intact and young bitches (P < 0.01, P < 0.01) and in animals with regular estrous periods (P = 0.03). Malignant tumors of the bitches with a previous clinical history of pseudopregnancy expressed significantly more ER-alpha (P = 0.04). Immunoexpression of ER-alpha decreased significantly with tumor size (P = 0.05) and skin ulceration (P = 0.01). Low levels of ER-alpha were significantly associated with lymph node involvement (P < 0.01). Malignant tumors had lower ER-alpha expression than did benign tumors (P < 0.01). Proliferation index measured by proliferating cell nuclear antigen immunostaining was inversely correlated with ER-alpha scores (P = 0.05) in all tumors. Low ER-alpha levels in primary malignant tumors were significantly associated with the occurrence of metastases in the follow-up (P = 0.03). Multivariate analyses were performed to determine the prognostic significance of some follow-up variables. ER-alpha value, Ki-67 index, and age were independent factors that could predict disease-free survival. Lymph node status, age, and ER-alpha index were independent prognostic factors for the overall survival. The immunohistochemical detection of ER-alpha in canine mammary tumors is a simple technique with prognostic value that could be useful in selecting appropriate hormonal therapy.
Peak bone mass has been shown to be a significant predictor of risk for osteoporosis. Previous studies have demonstrated that skeletal mass accumulation is under strong genetic control, and efforts have been made to identify candidate loci. Determinants of peak bone mass also include diet, physical activity, hormonal status, and other clinical factors. The overall contribution of these factors, genetic and nongenetic, and their interaction in determining peak bone density status have not been delineated. Six hundred and seventy-seven healthy unrelated Caucasian women ages 18-35 years were assessed. A detailed, standardized interview was conducted to evaluate lifestyle factors, menstrual and reproductive history, medical conditions, medication use, and family history of osteoporosis. Bone mineral density (BMD) was measured at the lumbar spine (L2-L4) and the femoral neck (hip) using dual-energy X-ray absorptiometry. Genotyping of the vitamin D receptor (VDR) locus at three polymorphic sites (BsmI, ApaI, and TaqI) was performed. In bivariate analyses, BMD at the lumbar spine and hip was positively correlated with weight, height, body mass index (BMI), and level of physical activity, both now and during adolescence, but negatively correlated with a family history of osteoporosis. Hip, but not spine BMD, correlated positively with dietary intake of calcium, and negatively with amenorrhea of more than 3 months, with caffeine intake, and with age. Spine, but not hip BMD, correlated positively with age and with number of pregnancies. VDR haplotype demonstrated significant associations with BMD at the hip, level of physical activity currently, and BMI. In multivariate analysis, independent predictors of greater BMD (at the hip or spine) were: age (younger for the hip, older for the spine), greater body weight, greater height (hip only), higher level of physical activity now and during adolescence, no family history of osteoporosis, and VDR genotype (hip only). Weight, age, level of physical activity, and family history are independent predictors of peak BMD. Of these factors, weight accounts for over half the explained variability in BMD. VDR alleles are significant independent predictors of peak femoral neck, but not lumbar spine BMD, even after adjusting for family history of osteoporosis, weight, age, and exercise. However, the overall contribution of this genetic determinant is modest. Taken together, these factors explained approximately 17% and 21% of the variability in peak spine and hip BMD, respectively, in our cohort. Future research should be aimed at further evaluation of genetic determinants of BMD. Most importantly, understanding the critical interactive nature between genes and the environment will facilitate development of targeted strategies directed at modifying lifestyle factors as well as earlier intervention in the most susceptible individuals.
A questionnaire was mailed to dentists and dental assistants requesting information about work, health, and reproductive history. Statistical analysis of the data indicated that there were no increased rates of spontaneous abortions or congenital abnormalities in the children of men and women who were exposed to low versus high levels of mercury in a dental environment.
Lung cancer results from man-made and natural environmental exposures acting in concert with both genetic and acquired characteristics. Chronic inhalation of cigarette smoke is a major risk factor, and environmental tobacco exposure can cause lung cancer in life-long neversmokers. Air pollution, indoor-radon exposure, occupational exposures, dietary, physical activity, and reproductive history have been identified as independent or contributing risk factors for lung cancer. Because only a small portion of smokers develops the disease, genetic susceptibility can contribute to the risk. Developments in molecular biology have led to the discovery of biological markers that increase predisposition to lung carcinogenesis. Therefore, the high-risk genotype of an individual can be determined easily. Because of the great number of carcinogen-activating and -detoxifying enzymes, the variation in their expression, the complexity of exposures to tobacco carcinogens, and the existence of multiple alleles at loci of those enzymes results in differential susceptibilities of individuals. As lung cancer is a multifactorial disease, an improved understanding of the interplay of environmental and genetic polymorphisms at multiple loci can help identify individuals who are at increased risk for lung cancer. Hopefully, in the future we will be able to screen for lung cancer susceptibility by using specific biomarkers.
This article critiques medical ecological analysis of female circumcision as a "maladaptive cultural pattern" and argues that this highly controversial procedure must be analyzed within the larger contexts of women's lives in underdeveloped countries. International efforts to eradicate female circumcision, while often couched in seemingly progressive feminist rhetoric, inadvertently serve to mask the negative health effects of the economic exploitation of poor countries such as Sudan. Reproductive histories and ethnographic data are used to argue that though female circumcision is not maladaptive, cultural discourse about it is resulting in changes in the meaning, techniques, and frequency of this practice.
Cows of normal reproductive history were treated with progesterone for periods of 2--3 months. The uterine secretions yielded 5 major fractions of macromolecular components. Two of the fractions comprised serum proteins. In the other 3 fractions at least 9 non-serum proteins were observed, 7 in one fraction, but in only small amounts. Of the remaining 2 non-serum proteins one is an acid phosphatase recoverable in small amounts, and the other is lactoferrin and is the major non-serum protein present in the uterine secretions of progesterone-treated cows.
This study compares socio-demographic factors, mothers' biological characteristics, and quality of care at maternity hospitals in the City of Rio de Janeiro, Brazil. A sample of 10,072 post-partum women in 47 hospitals was selected. Data were collected by interviewing mothers in the immediate post-partum and from medical records. The chi2 test was used to analyze homogeneity of ratios. Significant differences were found between patients in public and private hospitals in relation to family support, healthy habits during pregnancy, reproductive history, access to and satisfaction with prenatal care and delivery, and particularly adverse effects in the newborns. Private maternity hospitals showed better results, although they displayed excessive cesarean and neonatal inter-hospital transfer rates. The stratum consisting of public Federal and State maternity hospitals received women with greater morbidity, had lower neonatal transfer rates, and received a more positive assessment by clients of the Unified National Health System (SUS). Private maternity centers contracted out by the SUS were the ones that most refused treatment to patients, leading to delays in patient care for delivery.