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Biomedical subjects

J M Samet

Publications and source records attributed to J M Samet.

At least 73 records · Page 4Linked to original sources
PubMed1999

Frequency of policy recommendations in epidemiologic publications.

OBJECTIVES: The purpose of this study was to determine the frequency and character of policy statements in epidemiologic reports. METHODS: The first author followed a standardized protocol and reviewed a random sample of articles selected from the American Journal of Epidemiology, Annals of Epidemiology, and Epidemiology. The second author reviewed all articles with policy statements and a 10% sample without such statements. RESULTS: Overall, 23.8% of the articles contained policy statements. Annals of Epidemiology and the American Journal of Epidemiology had similar frequencies of articles with policy statements (30% and 26.7%, respectively), while Epidemiology evidenced the lowest frequency (8.3%). The majority of policy statements (55%) pertained to public health practice; 27.5% involved clinical practice, and the remainder (17.5%) focused on corporate policies, regulatory actions, or undefined arenas. The frequency of policy statements differed according to first author's affiliation, type of publication, area of research, research design, and study population. CONCLUSIONS: Although a minority of publications included policy statements, the inclusion of a statement seemed to be influenced by specific study characteristics.

Adolescent↗
PubMed1998

Reproductive risk factors for breast cancer in Hispanic and non-Hispanic white women: the New Mexico Women's Health Study.

The authors conducted a population-based case-control study of breast cancer in Hispanic women in New Mexico. Hispanic and non-Hispanic white women with incident breast cancer, aged 30-74 years and diagnosed between 1992 and 1994, were identified by the New Mexico Tumor Registry. Controls were selected using random digit dialing and frequency matched by ethnicity, age, and region. Information on reproductive history, lactation, and other risk factors was collected through in-person interviews; 719 Hispanics and 836 non-Hispanic whites were included in the analysis. Conditional logistic regression was used to estimate relative risk of breast cancer for reproductive factors and to assess ethnic differences in effects. Older age at first full-term birth was associated with breast cancer among Hispanics; the odds ratio for women aged 27 years and older at first full-term birth compared with women 18 years or younger was 2.26 (95% confidence interval 1.17-4.38) compared with 1.60 (95% confidence interval 0.86-3.01) for non-Hispanic whites. Higher parity was associated with reduced risk of breast cancer for non-Hispanic whites, but not Hispanics (p < 0.008). Longer lactation was associated with reduced risk in premenopausal Hispanic women and premenopausal and postmenopausal non-Hispanic white women. Reproductive factors explained 17% of the ethnic difference in breast cancer incidence for postmenopausal women and none of the difference for premenopausal women.

Adult↗
PubMed1998

Mechanisms that account for the selective release of arachidonic acid from intact cells by secretory phospholipase A2.

The current study examined mechanisms that account for the selective release of arachidonic acid (AA) from cells by secretory phospholipase A2 (sPLA2). Initial studies demonstrated that low concentrations of group I and group III PLA2 isotypes and an sPLA2-enriched extract from bone marrow-derived mast cells (BMMC) selectively released AA from mast cells. Much higher concentrations of group II PLA2 were required to release comparable quantities of AA. Group I PLA2 also selectively released AA from another mast cell line (CFTL-15) and a monocytic cell line (THP-1). In contrast, high concentrations of group I PLA2 were required to release fatty acids from a promyelocytic cell line (HL-60) and this release was not selective for AA. Binding studies revealed that cell types (BMMC, CFTL-15 and THP-1) which selectively released AA also had the capacity to specifically bind group I PLA2. However, group II PLA2, which did not selectively release AA from cells, also did not specifically bind to these same cell types. Additional studies revealed that sPLA2 binding to the mast cell receptor was attenuated after stimulation with antigen or ionophore A23187. Reverse transcriptase-polymerase chain reaction analyses indicated the presence of mRNA for the sPLA2 receptor in BMMC, CFTL-15 and THP-1 and the absence of this mRNA in HL-60. Final studies demonstrated that p-aminophenyl-alpha-D-mannopyranoside BSA, a known ligand of the sPLA2 receptor, also selectively released AA from mast cells but not from HL-60 cells. These experiments indicated that receptor occupancy alone (without PLA2 activity) is sufficient to induce the release of AA from mast cells. Together, these data reveal that specific isotypes of sPLA2 have the capacity to selectively release AA from certain cells by their capacity to bind to sPLA2 receptors on the cell surface.

Animals↗
PubMed1998

Breastfeeding reduces risk of respiratory illness in infants.

Breastfeeding has long been believed to protect against infection in infants, but protection against respiratory illnesses has not been consistently demonstrated in studies in developed countries. Between 1988 and 1992, the authors assessed the effect of breastfeeding on incidence and duration of respiratory illnesses during the first 6 months of life in a prospective study that actively tracked breastfeeding and respiratory illnesses. A cohort of 1,202 healthy infants, born in Albuquerque, New Mexico, between January 1, 1988 and June 30, 1990, from homes without smokers was enrolled. The daily occurrences of respiratory symptoms and breastfeeding status were reported by the mothers every 2 weeks. Illnesses were classified as lower respiratory illness (LRI) if wheezing or wet cough was reported; the remaining illnesses were classified as upper respiratory. The annualized incidence rates for LRI were 2.8, 2.6, and 2.1 during follow-up time with no, partial, or full breastfeeding, respectively, but the incidence rates for upper respiratory illness and lower respiratory illness combined were similar in the three categories. After adjustment for potential confounding factors, full breastfeeding was associated with a reduction in lower respiratory illness risk (odds ratio=0.81, 95% confidence interval 0.68-0.96). Median duration of all respiratory illnesses was 5 days for the fully breastfed infants during the first 6 months of life compared with a median of 6 days for not breastfed and partially breastfed infants. Multivariate analysis confirmed that breastfeeding significantly reduced the duration of respiratory illness. This pattern of reduced incidence of LRI and shorter duration of all respiratory illnesses suggests that breastfeeding reduces the severity of infant respiratory illnesses during the first 6 months of life.

Adolescent↗
PubMed1998

Idiopathic pulmonary fibrosis: survival in population based and hospital based cohorts.

BACKGROUND: To ascertain whether findings from hospital based clinical series can be extended to patients with idiopathic pulmonary fibrosis (IPF) in the general population, the survival of patients with IPF in a population based registry was compared with that of a cohort of patients with IPF treated at major referral hospitals and the factors influencing survival in the population based registry were identified. METHODS: The survival of 209 patients with IPF from the New Mexico Interstitial Lung Disease Registry and a cohort of 248 patients with IPF who were participating in a multicentre case-control study was compared. The determinants of survival for the patients from the Registry were determined using life table and proportional hazard modelling methods. RESULTS: The median survival times of patients with IPF in the Registry and case-control cohorts were similar (4.2 years and 4.1 years, respectively), although the average age at diagnosis of the Registry patients was greater (71.7 years versus 60.6 years, p < 0.01). After adjusting for differences in age, sex, and ethnicity, the death rate within six months of diagnosis was found to be greater in the Registry patients (relative hazard (RH) 6.32, 95% CI 2.19 to 18.22) but more than 18 months after diagnosis the death rate was less (RH 0.35, 95% CI 0.19 to 0.66) than in the patients in the case-control study. Factors associated with poorer prognosis in the Registry included advanced age, severe radiographic abnormalities, severe reduction in forced vital capacity, and a history of corticosteroid treatment. CONCLUSIONS: The adjusted survival of patients with IPF in the general population is different from that of hospital referrals which suggests that selection biases affect the survival experience of referral hospitals.

Aged↗
PubMed1998

Metal-dependent expression of ferritin and lactoferrin by respiratory epithelial cells.

Increased availability of catalytically active metal has been associated with an oxidative injury. The sequestration of transition metals within intracellular ferritin confers an antioxidant function to this protein. Such storage by ferritin requires that the metal be transported across a cell membrane. We tested the hypothesis that, in response to in vitro exposures to catalytically active metal, respiratory epithelial cells increase the production of lactoferrin and ferritin to bind, transport, and store this metal with their coordination sites fully complexed. Residual oil fly ash is an emission source air pollution particle with biological effects that, both in vitro and in vivo, correspond with its metal content. Cell cultures were exposed to 0-200 micrograms/ml of oil fly ash for 2 and 24 h. Concentrations of ferritin and lactoferrin mRNA were estimated by reverse transcription-polymerase chain reaction, and concentrations of ferritin and lactoferrin proteins were measured in parallel. mRNA for ferritin did not change with exposure to oil fly ash. However, ferritin protein concentrations increased. Although mRNA for transferrin receptor decreased, mRNA for lactoferrin increased after incubation with the particle. Similar to changes in mRNA, transferrin concentration decreased, whereas that of lactoferrin increased. Deferoxamine, a metal chelator, inhibited these responses, and exposure of the cells to vanadium compounds alone reproduced elevations in lactoferrin mRNA. We conclude that increases in ferritin and lactoferrin expression can be metal dependent. This response can function to diminish the oxidative stress a metal chelate presents to a living system.

Air Pollutants↗
PubMed1998

Activation of MAPKs in human bronchial epithelial cells exposed to metals.

We have previously shown that in vitro exposure to metallic compounds enhances expression of interleukin (IL)-6, IL-8, and tumor necrosis factor-alpha in human bronchial epithelial cells. To characterize signaling pathways involved in metal-induced expression of inflammatory mediators and to identify metals that activate them, we studied the effects of As, Cr, Cu, Fe, Ni, V, and Zn on the mitogen-activated protein kinases (MAPK) extracellular receptor kinase (ERK), c-Jun NH2-terminal kinase (JNK), and P38 in BEAS cells. Noncytotoxic concentrations of As, V, and Zn induced a rapid phosphorylation of MAPK in BEAS cells. Activity assays confirmed marked activation of ERK, JNK, and P38 in BEAS cells exposed to As, V, and Zn. Cr and Cu exposure resulted in a relatively small activation of MAPK, whereas Fe and Ni did not activate MAPK under these conditions. Similarly, the transcription factors c-Jun and ATF-2, substrates of JNK and P38, respectively, were markedly phosphorylated in BEAS cells treated with As, Cr, Cu, V, and Zn. The same acute exposure to As, V, or Zn that activated MAPK was sufficient to induce a subsequent increase in IL-8 protein expression in BEAS cells. These data suggest that MAPK may mediate metal-induced expression of inflammatory proteins in human bronchial epithelial cells.

Activating Transcription Factor 2↗
PubMed1998

Validity and reproducibility of a food frequency questionnaire among Hispanic and non-Hispanic white women in New Mexico.

The purpose of this study was to assess the validity and reproducibility of an interviewer-administered, semi-quantitative food frequency questionnaire (FFQ) among 132 volunteer New Mexico Hispanic (H) and non-Hispanic white (NHW) women, aged 35-74 years, with (n = 47) and without (n = 85) a breast cancer history, and to add to the limited data presently available on the performance of FFQs among different ethnic groups. Validity was measured at one month and six months from baseline against four-day food records, and reproducibility was tested by comparing FFQs. Unadjusted validity correlation coefficients were highest at one month, ranging from 0.38 (polyunsaturated and monounsaturated fat) to 0.57 (calcium); energy-adjusted correlation coefficients were highest at six months, ranging from 0.15 (polyunsaturated fat) to 0.68 (calcium). Energy-adjusted correlation coefficients were statistically significant by ethnicity for vitamins A and C, protein, carotene and calcium, and by case status for saturated fat, folate, fiber, and vitamins A and E. Reproducibility correlation coefficients (unadjusted) ranged from 0.40 (polyunsaturated fat) to 0.71 (carbohydrate, retinol); energy-adjusted correlation coefficients ranged from 0.42 (vitamin E) to 0.78 (fiber), and differed significantly by ethnicity for saturated fat and retinol, and by case status for carbohydrate. Overall, our FFQ has comparable characteristics to other FFQs and is suitable for use with New Mexico's H and NHW women.

Adult↗
PubMed1997

Air pollution and mortality in Philadelphia, 1974-1988.

Analyses involving data from many locations throughout the world have now been conducted to assess the association between air pollution and mortality. To date, six independent analyses of mortality data for Philadelphia, Pennsylvania, have been reported. In this new analysis of Philadelphia data for 1974-1988, Poisson regression models were developed to estimate the increased risk of daily mortality associated with air pollution while controlling for longer-term time trends and season and for weather. Model development was based on prior understanding of the effects of these factors on mortality and on consideration of model fit. The authors found moderate correlations of daily concentrations of total suspended particles (TSP), sulfur dioxide (SO2), nitrogen dioxide (NO2), and carbon monoxide (CO), and only slight correlations of ozone (O3) with other pollutants. When included individually in the model, the means of current and previous days' levels of TSP, SO2, and O3 had statistically significant effects on total mortality; pollutant increases of an interquartile range (34.5 micrograms/m3, 12.9 ppb, and 20.2 ppb, respectively) were associated with increases in mortality of around 1% for TSP and SO2, and of around 2% for O3. The effects of TSP and SO2 were diminished when both pollutants were simultaneously included in the model, whether pairwise or in the full multi-pollutant model. These analyses confirm the association between TSP and mortality found in previous studies in Philadelphia and show that the association is robust to consideration of other pollutants in the model.

Aged↗
PubMed1997

Molecular damage in the bronchial epithelium of current and former smokers.

BACKGROUND: Most lung cancers are attributed to smoking. These cancers have been associated with multiple genetic alterations and with the presence of preneoplastic bronchial lesions. In view of such associations, we evaluated the status of specific chromosomal loci in histologically normal and abnormal bronchial biopsy specimens from current and former smokers and specimens from nonsmokers. METHODS: Multiple biopsy specimens were obtained from 18 current smokers, 24 former smokers, and 21 nonsmokers. Polymerase chain reaction-based assays involving 15 polymorphic microsatellite DNA markers were used to examine eight chromosomal regions for genetic changes (loss of heterozygosity [LOH] and microsatellite alterations). RESULTS: LOH and microsatellite alterations were observed in biopsy specimens from both current and former smokers, but no statistically significant differences were observed between the two groups. Among individuals with a history of smoking, 86% demonstrated LOH in one or more biopsy specimens, and 24% showed LOH in all biopsy specimens. About half of the histologically normal specimens from smokers showed LOH, but the frequency of LOH and the severity of histologic change did not correspond until the carcinoma in situ stage. A subset of biopsy specimens from smokers that exhibited either normal or preneoplastic histology showed LOH at multiple chromosomal sites, a phenomenon frequently observed in carcinoma in situ and invasive cancer. LOH on chromosomes 3p and 9p was more frequent than LOH on chromosomes 5q, 17p (17p13; TP53 gene), and 13q (13q14; retinoblastoma gene). Microsatellite alterations were detected in 64% of the smokers. No genetic alterations were detected in nonsmokers. CONCLUSIONS: Genetic changes similar to those found in lung cancers can be detected in the nonmalignant bronchial epithelium of current and former smokers and may persist for many years after smoking cessation.

Adult↗
PubMed1997

Cytokine production by human airway epithelial cells after exposure to an air pollution particle is metal-dependent.

Despite the many epidemiological studies supporting the contention that ambient air pollution particles can adversely affect human health, there is no clear agreement as to a biologically plausible mechanism which can explain the acute mortality and morbidity associated with exposure to particles less than 10 microm in size. We tested the hypothesis that metals present in an air pollution particle can induce the synthesis and expression of the inflammatory cytokines IL-8, IL-6, and TNFalpha. A residual oil fly ash (ROFA) containing the transition metals vanadium, nickel, and iron was used as a model emission source air pollution particle. Normal human bronchial epithelial (NHBE) cells were exposed for either 2 or 24 hr to 0, 5, 50, or 200 microg/ml ROFA. Concentrations of IL-8, IL-6, and TNF-alpha proteins were measured with commercially available ELISA kits. mRNA for these same cytokines was quantified by RT-PCR. NHBE cells exposed to ROFA produced significant amounts of IL-8, IL-6, and TNF, as well as mRNAs coding for these cytokines. Cytokine production was inhibited by the inclusion of either the metal chelator deferoxamine (1.0 mM) or the free radical scavenger dimethylthiourea (1.0 mM). In addition, vanadium containing compounds, but not iron or nickel sulfates, mimicked the effects of intact ROFA. These results demonstrate that metals present in ROFA may be responsible for production and release of inflammatory mediators by the respiratory tract epithelium and suggest that these mediators may contribute to the toxic effects of particulate air pollutants reported in epidemiology studies.

Air Pollutants, Occupational↗