Measuring Variation in Interpregnancy Interval: Identifying Hotspots for Improvement Initiatives.

OBJECTIVE: The study aimed to determine if single year birth certificate data can be used to identify regional and hospital variation in rates of short interpregnancy interval (IPI < 6 months). STUDY DESIGN: IPI was estimated for multiparous women ages 15 to 44 years with singleton live births between 2015 and 2016. Perinatal outcomes, place of birth, maternal race, and data for IPI calculations were obtained by using birth certificates. IPI frequencies are presented as observed rates. RESULTS: The cohort included 562,039 multiparous women. Short IPI rates were similar to those obtained with analyses by using linked longitudinal data and confirmed the association with preterm birth. Short IPI rates varied by race and Hispanic nativity. There was substantial hospital (0.8-9%) and regional (2.9-6.2%) variation in short IPI rates. CONCLUSION: IPI rates can be reliably obtained from current year birth certificate data. This can be a useful tool for quality improvement projects targeting interventions and rapidly assessing their progress to promote optimal birth spacing. KEY POINTS: · Near-real time regional and hospital IPI rates can be reliably obtained from current year birth certificate data.. · Substantial variations in rates of short IPI exist between hospital and perinatal regions.. · IPI rates from individual birth certificates can be a tool to target and assess interventions..

Hospital Quality Improvement Interventions, Statewide Policy Initiatives, and Rates of Cesarean Delivery for Nulliparous, Term, Singleton, Vertex Births in California.

Importance: Safe reduction of the cesarean delivery rate is a national priority. Objective: To evaluate the rates of cesarean delivery for nulliparous, term, singleton, vertex (NTSV) births in California in the context of a statewide multifaceted intervention designed to reduce the rates of cesarean delivery. Design, Setting, and Participants: Observational study of cesarean delivery rates from 2014 to 2019 among 7 574 889 NTSV births in the US and at 238 nonmilitary hospitals providing maternity services in California. From 2016 to 2019, California Maternal Quality Care Collaborative partnered with Smart Care California to implement multiple approaches to decrease the rates of cesarean delivery. Hospitals with rates of cesarean delivery greater than 23.9% for NTSV births were invited to join 1 of 3 cohorts for an 18-month quality improvement collaborative between July 2016 and June 2019. Exposures: Within the collaborative, multidisciplinary teams implemented multiple strategies supported by mentorship, shared learning, and rapid-cycle data feedback. Partnerships among nonprofit organizations, state governmental agencies, purchasers, and health plans addressed the external environment through transparency, award programs, and incentives. Main Outcomes and Measures: The primary outcome was the change in cesarean delivery rates for NTSV births in California and a difference-in-differences analysis was performed to compare cesarean delivery rates for NTSV births in California vs the rates in the rest of the US. A mixed multivariable logistic regression model that adjusted for patient-level and hospital-level confounders also was used to assess the collaborative and the external statewide actions. The cesarean delivery rates for NTSV births at hospitals participating in the collaborative were compared with the rates from the nonparticipating hospitals and the rates in the participating hospitals prior to participation in the collaborative. Results: A total of 7 574 889 NTSV births occurred in the US from 2014 to 2019, of which 914 283 were at 238 hospitals in California. All California hospitals were exposed to the statewide actions to reduce the rates of cesarean delivery, including the 149 hospitals that had baseline rates of cesarean delivery greater than 23.9% for NTSV births, of which 91 (61%) participated in the quality improvement collaborative. The rate of cesarean delivery for NTSV births in California decreased from 26.0% (95% CI, 25.8%-26.2%) in 2014 to 22.8% (95% CI, 22.6%-23.1%) in 2019 (relative risk, 0.88; 95% CI, 0.87-0.89). The rate of cesarean delivery for NTSV births in the US (excluding California births) was 26.0% in both 2014 and 2019 (relative risk, 1.00; 95% CI, 0.996-1.005). The difference-in-differences analysis revealed that the reduction in the rate of cesarean delivery for NTSV births in California was 3.2% (95% CI, 1.7%-3.5%) higher than in the US (excluding California). Compared with the hospitals and the periods not exposed to the collaborative activities, and after adjusting for patient characteristics and time using a modified stepped-wedge analysis, exposure to collaborative activities was associated with a lower odds of cesarean delivery for NTSV births (24.4% vs 24.6%; adjusted odds ratio, 0.87 [95% CI, 0.85-0.89]). Conclusions and Relevance: In this observational study of NTSV births in California from 2014 to 2019, the rates of cesarean delivery decreased over time in the setting of the implementation of a coordinated hospital-level collaborative and statewide initiatives designed to support vaginal birth.

Reduction in racial disparities in severe maternal morbidity from hemorrhage in a large-scale quality improvement collaborative.

BACKGROUND: Eliminating persistent racial/ethnic disparities in maternal mortality and morbidity is a public health priority. National strategies to improve maternal outcomes are increasingly focused on quality improvement collaboratives. However, the effectiveness of quality collaboratives for reducing racial disparities in maternity care is understudied. OBJECTIVE: To evaluate the impact of a hemorrhage quality-improvement collaborative on racial disparities in severe maternal morbidity from hemorrhage. STUDY DESIGN: We conducted a cross-sectional study from 2011 to 2016 among 99 hospitals that participated in a hemorrhage quality improvement collaborative in California. The focus of the quality collaborative was to implement the national maternal hemorrhage safety bundle consisting of 17 evidence-based recommendations for practice and care processes known to improve outcomes. This analysis included 54,311 women from the baseline period (January 2011 through December 2014) and 19,165 women from the postintervention period (October 2015 through December 2016) with a diagnosis of obstetric hemorrhage during delivery hospitalization. We examined whether racial/ethnic-specific severe maternal morbidity rates in these women with obstetric hemorrhage were reduced from the baseline to the postintervention period. In addition, we conducted Poisson Generalized Estimating Equation models to estimate relative risks and 95% confidence intervals for severe maternal morbidity comparing each racial/ethnic group with white. RESULTS: During the baseline period, the rate of severe maternal morbidity among women with hemorrhage was 22.1% (12,002/54,311) with the greatest rate observed among black women (28.6%, 973/3404), and the lowest among white women (19.8%, 3124/15,775). The overall rate fell to 18.5% (3553/19,165) in the postintervention period. Both black and white mothers benefited from the intervention, but the benefit among black women exceeded that of white women (9.0% vs 2.1% absolute rate reduction). The baseline risk of severe maternal morbidity was 1.34 times greater among black mothers compared with white mothers (relative risk, 1.34; 95% confidence interval, 1.27-1.42), and it was reduced to 1.22 (1.05-1.40) in the postintervention period. Sociodemographic and clinical factors explained a part of the black-white differences. After controlling for these factors, the black-white relative risk was 1.22 (95% confidence interval, 1.15-1.30) at baseline and narrowed to 1.07 (1.92-1.24) in the postintervention period. Results were similar when excluding severe maternal morbidity cases with transfusion alone. After accounting for maternal risk factors, the black-white relative risk for severe maternal morbidity excluding transfusion alone was reduced from a baseline of 1.33 (95% confidence interval, 1.16-1.52) to 0.99 (0.76-1.29) in the postintervention period. The most important clinical risk factor for disparate black rates for both severe maternal morbidity and severe maternal morbidity excluding transfusion alone was cesarean delivery, potentially providing another opportunity for quality improvement. CONCLUSION: A large-scale quality improvement collaborative reduced rates of severe maternal morbidity due to hemorrhage in all races and reduced the performance gap between black and white women. Improving access to highly effective treatments has the potential to decrease disparities for care-sensitive acute hospital-focused morbidities.

Trends in Statin Use 2009-2015 in a Large Integrated Health System: Pre- and Post-2013 ACC/AHA Guideline on Treatment of Blood Cholesterol.

PURPOSE: Implementation of the 2013 ACC/AHA cholesterol treatment guideline is likely to vary by statin benefit group. The aim of this study was to document trends in statin use before and after introduction of the ACC/AHA guideline. METHODS: We conducted a retrospective study with annual cohorts from 2009 to 2015 among members of Kaiser Permanente Southern California aged ≥ 21 years. Members were categorized into four mutually exclusive statin benefit groups: atherosclerotic cardiovascular disease (ASCVD), LDL-C ≥ 190 mg/dL in the last year, diabetes (aged 40-75 years), and 10-year ASCVD risk ≥ 7.5% (aged 40-75 years). RESULTS: The cohorts ranged from 1,993,755 members in 2009 to 2,440,429 in 2015. Approximately 5% of patients had ASCVD, 1% had LDL-C ≥ 190 mg/dL, 6% had diabetes, and 10% had a 10-year ASCVD risk ≥ 7.5% each year. Trends in statin use were stable for adults with ASCVD (2009 78%; 2015 80%), recent LDL-C ≥ 190 mg/dL (2009 45%; 2015 44%), and diabetes (2009 74%; 2015 73%), but increased for patients with 10-year ASCVD risk ≥ 7.5% (2009 36%; 2015 47%). High-intensity statin use also increased 142% and 54% among patients with LDL-C ≥ 190 mg/dL and those with ASCVD ≤ 75 years of age, respectively. Moderate-to-high intensity statin utilization increased over 50% among those with a 10-year ASCVD risk ≥ 7.5%. CONCLUSIONS: Statin use increased substantially among patients with 10-year ASCVD risk ≥ 7.5% and use of appropriate statin dosage increased in each of the four statin benefit groups between 2009 and 2015; however, there is room for improvement.

Improving Maternal Safety at Scale with the Mentor Model of Collaborative Improvement.

BACKGROUND: Obstetric safety bundles, consisting of action steps shown to improve outcomes, have been developed to address the most common and preventable causes of maternal morbidity and mortality. Implementing these best practices across all birthing facilities remains an important and challenging clinical and public health priority. METHODS: The California Maternal Quality Care Collaborative (CMQCC) developed an innovative external mentor model for large-scale collaborative improvement in which participating organizations were subdivided into small teams of six to eight hospitals, led by a paired dyad of physician and nurse leaders. The mentor model preserves the active sharing that enhances improvement across a large group of facilities working on the same project while enabling individualized attention to teams. The mentor model was tested by implementing the obstetric hemorrhage safety bundle (which consists of 17 key practices in four domains) in multiple California hospitals. RESULTS: A total of 126 hospitals were engaged to simultaneously implement the safety bundle. The adoption rates for the recommended practices in the four action domains were (1) Readiness, 78.9%; (2) Recognition and Prevention, 76.5%; (3) Response, 63.1%; and (4) Reporting and Systems Learning, 58.7%. Mentors (31/40) and participating teams (48 responses from 39/126 hospitals) provided feedback in an exit survey. Among the respondents, 64.5% of mentors and 72.9% of participants agreed that compared to a traditional collaborative structure, the mentor model was better suited for quality improvement at scale. CONCLUSION: The mentor model was successful in providing individualized support to teams and enabled implementation of the hemorrhage safety bundle across a diverse group of 126 hospitals.

Case-control study of cumulative cigarette tar exposure and lung and upper aerodigestive tract cancers.

The development of comprehensive measures for tobacco exposure is crucial to specify effects on disease and inform public health policy. In this population-based case-control study, we evaluated the associations between cumulative lifetime cigarette tar exposure and cancers of the lung and upper aerodigestive tract (UADT). The study included 611 incident cases of lung cancer; 601 cases of UADT cancers (oropharyngeal, laryngeal and esophageal cancers); and 1,040 cancer-free controls. We estimated lifetime exposure to cigarette tar based on tar concentrations abstracted from government cigarette records and self-reported smoking histories derived from a standardized questionnaire. We analyzed the associations for cumulative tar exposure with lung and UADT cancer, overall and according to histological subtype. Cumulative tar exposure was highly correlated with pack-years among ever smoking controls (Pearson coefficient = 0.90). The adjusted odds ratio (95% confidence limits) for the estimated effect of about 1 kg increase in tar exposure (approximately the interquartile range in all controls) was 1.61 (1.50, 1.73) for lung cancer and 1.21 (1.13, 1.29) for UADT cancers. In general, tar exposure was more highly associated with small, squamous and large cell lung cancer than adenocarcinoma. With additional adjustment for pack-years, positive associations between tar and lung cancer were evident, particularly for small cell and large cell subtypes. Therefore, incorporating the composition of tobacco carcinogens in lifetime smoking exposure may improve lung cancer risk estimation. This study does not support the claim of a null or inverse association between "low exposure" to tobacco smoke and risk of these cancer types.

Association of sugary beverages with survival among patients with cancers of the upper aerodigestive tract.

PURPOSE: The role of consumption of added sugars in cancers of the upper aerodigestive tract (UADT) is unclear. We examined associations between sugary beverages and susceptibility to UADT cancer as well as overall survival among UADT cancer patients. METHODS: The association between dietary added sugar and susceptibility to UADT cancers or overall survival among 601 UADT cancer cases was evaluated using data from a population-based case-control study conducted in Los Angeles County. Unconditional logistic regression was used to estimate odds ratios and 95 % confidence intervals (CI) for cancer susceptibility, and Cox regression was used to estimate hazards ratios (HRs) with 95 % CIs for survival, adjusting for relevant confounders. RESULTS: A total of 248 deaths were observed during follow-up (median 12.1 years). A positive association was observed with consumption of grams of sugar from beverages, including soft drinks and fruit juices, and poorer survival among UADT cancer cases (aHR, Q4 vs. Q1:1.88; 95 % CI 1.29, 2.72; p for trend = 0.002), as well as servings of sugary beverages (aHR, Q4 vs. Q1: 95 % CI 1.97, 95 % CI 1.32-2.93). This was due largely to consumption of sugars from soft drinks. Particularly, high consumption of sugary beverages was associated with poorer survival among esophageal cancer cases, driven by squamous cancers. No association was observed between sugary beverages and cancer susceptibility. CONCLUSION: These findings suggest that consumption of sugary beverages may decrease survival associated with UADT cancers. Additional studies should be conducted to examine survival among cancer patients consuming high amounts of added or refined sugars. Such studies may highlight prognostic factors for UADT cancers.

Association between PNPLA3 (rs738409), LYPLAL1 (rs12137855), PPP1R3B (rs4240624), GCKR (rs780094), and elevated transaminase levels in overweight/obese Mexican adults.

There is scarce information about the link between specific single-nucleotide polymorphisms (SNPs) and risk of liver disease among Latinos, despite the disproportionate burden of disease among this population. Our aim was to investigate nine SNPs in or near the following genes: PNPLA3, LYPLAL1, PPP1R3B, GCKR, NCAN, IRS1, PPARG, and ADIPOR2 and examine their association with persistently elevated alanine aminotransferase (ALT) or aspartate aminotransferase (AST) levels in Mexican adults. Data and samples were collected from 741 participants in the Mexican Health Worker Cohort Study, in Cuernavaca, Mexico. We identified 207 cases who had persistently elevated levels of ALT or AST (≥40 U/L) and 534 controls with at least two consecutive normal ALT or AST results in a 6 month period, during 2004-2006 and 2011-2013. TaqMan assays were used to genotype the SNPs. The risk allele of PNPLA3 rs738409 was found to be associated with persistently elevated levels of ALT or AST, adjusting for age, sex, BMI, type 2 diabetes, and ancestry: (OR 2.28, 95 % CI 1.13, 4.58). A significant association was found between the LYPLAL1, PPP1R3B, and GCKR risk alleles and elevated ALT or AST levels among overweight/obese adults. These results suggest that among Mexicans, the PNPLA3 (rs738409), LYPLAL1 (rs12137855), PPP1R3B (rs4240624), and GCKR (rs780094) polymorphisms may be associated with a greater risk of chronic liver disease among overweight adults. This study is the first to examine these nine SNPs in a sample of adults in Mexico.

Cannabis smoking and lung cancer risk: Pooled analysis in the International Lung Cancer Consortium.

To investigate the association between cannabis smoking and lung cancer risk, data on 2,159 lung cancer cases and 2,985 controls were pooled from 6 case-control studies in the US, Canada, UK, and New Zealand within the International Lung Cancer Consortium. Study-specific associations between cannabis smoking and lung cancer were estimated using unconditional logistic regression adjusting for sociodemographic factors, tobacco smoking status and pack-years; odds-ratio estimates were pooled using random effects models. Subgroup analyses were done for sex, histology and tobacco smoking status. The shapes of dose-response associations were examined using restricted cubic spline regression. The overall pooled OR for habitual versus nonhabitual or never users was 0.96 (95% CI: 0.66-1.38). Compared to nonhabitual or never users, the summary OR was 0.88 (95%CI: 0.63-1.24) for individuals who smoked 1 or more joint-equivalents of cannabis per day and 0.94 (95%CI: 0.67-1.32) for those consumed at least 10 joint-years. For adenocarcinoma cases the ORs were 1.73 (95%CI: 0.75-4.00) and 1.74 (95%CI: 0.85-3.55), respectively. However, no association was found for the squamous cell carcinoma based on small numbers. Weak associations between cannabis smoking and lung cancer were observed in never tobacco smokers. Spline modeling indicated a weak positive monotonic association between cumulative cannabis use and lung cancer, but precision was low at high exposure levels. Results from our pooled analyses provide little evidence for an increased risk of lung cancer among habitual or long-term cannabis smokers, although the possibility of potential adverse effect for heavy consumption cannot be excluded.

Associations of prostate cancer risk variants with disease aggressiveness: results of the NCI-SPORE Genetics Working Group analysis of 18,343 cases.

Genetic studies have identified single nucleotide polymorphisms (SNPs) associated with the risk of prostate cancer (PC). It remains unclear whether such genetic variants are associated with disease aggressiveness. The NCI-SPORE Genetics Working Group retrospectively collected clinicopathologic information and genotype data for 36 SNPs which at the time had been validated to be associated with PC risk from 25,674 cases with PC. Cases were grouped according to race, Gleason score (Gleason ≤ 6, 7, ≥ 8) and aggressiveness (non-aggressive, intermediate, and aggressive disease). Statistical analyses were used to compare the frequency of the SNPs between different disease cohorts. After adjusting for multiple testing, only PC-risk SNP rs2735839 (G) was significantly and inversely associated with aggressive (OR = 0.77; 95 % CI 0.69-0.87) and high-grade disease (OR = 0.77; 95 % CI 0.68-0.86) in European men. Similar associations with aggressive (OR = 0.72; 95 % CI 0.58-0.89) and high-grade disease (OR = 0.69; 95 % CI 0.54-0.87) were documented in African-American subjects. The G allele of rs2735839 was associated with disease aggressiveness even at low PSA levels (<4.0 ng/mL) in both European and African-American men. Our results provide further support that a PC-risk SNP rs2735839 near the KLK3 gene on chromosome 19q13 may be associated with aggressive and high-grade PC. Future prospectively designed, case-case GWAS are needed to identify additional SNPs associated with PC aggressiveness.

Plasma folate, vitamin B12, and homocysteine and cancers of the esophagus, stomach, and liver in a Chinese population.

Evidence is accumulating regarding a role of micronutrients in folate metabolism in cancer risk. We investigated the associations of plasma folate, vitamin B12, and homocysteine with upper gastrointestinal (GI) cancers in a population-based case-control study in Taixing City, China. With informed consent, we recruited cases with cancers of esophagus (n = 218), stomach (n = 206), and liver (n = 204), and one common healthy control group (n = 405). A standardized epidemiologic questionnaire was used in face-to-face interviews, and blood samples were collected during interviews. We observed an inverse association between plasma folate levels and liver cancer. The adjusted odds ratio (aOR) was 0.46 [95% confidence interval (CI) = 0.24-0.88] comparing individuals in the highest quartile to those in the lowest. We found a positive association between plasma vitamin B12 levels and all three cancers. The aORs for those in the highest quartile were 2.80 (95% CI = 1.51-5.18) for esophageal cancer, 2.17 (1.21-3.89) for stomach cancer, and 9.97 (4.82-20.60) for liver cancer, comparing to those in the lowest quartile. We further observed interaction between plasma folate and vitamin B12 on these cancers. Our data indicated associations between plasma folate and vitamin B12 with upper GI cancers in Chinese population. Further research is warranted considering the debate over the necessity of food fortification.

Exposure to secondhand tobacco smoke and lung cancer by histological type: a pooled analysis of the International Lung Cancer Consortium (ILCCO).

While the association between exposure to secondhand smoke and lung cancer risk is well established, few studies with sufficient power have examined the association by histological type. In this study, we evaluated the secondhand smoke-lung cancer relationship by histological type based on pooled data from 18 case-control studies in the International Lung Cancer Consortium (ILCCO), including 2,504 cases and 7,276 control who were never smokers and 10,184 cases and 7,176 controls who were ever smokers. We used multivariable logistic regression, adjusting for age, sex, race/ethnicity, smoking status, pack-years of smoking, and study. Among never smokers, the odds ratios (OR) comparing those ever exposed to secondhand smoke with those never exposed were 1.31 (95% CI: 1.17-1.45) for all histological types combined, 1.26 (95% CI: 1.10-1.44) for adenocarcinoma, 1.41 (95% CI: 0.99-1.99) for squamous cell carcinoma, 1.48 (95% CI: 0.89-2.45) for large cell lung cancer, and 3.09 (95% CI: 1.62-5.89) for small cell lung cancer. The estimated association with secondhand smoke exposure was greater for small cell lung cancer than for nonsmall cell lung cancers (OR=2.11, 95% CI: 1.11-4.04). This analysis is the largest to date investigating the relation between exposure to secondhand smoke and lung cancer. Our study provides more precise estimates of the impact of secondhand smoke on the major histological types of lung cancer, indicates the association with secondhand smoke is stronger for small cell lung cancer than for the other histological types, and suggests the importance of intervention against exposure to secondhand smoke in lung cancer prevention.

Tobacco smoking, NBS1 polymorphisms, and survival in lung and upper aerodigestive tract cancers with semi-Bayes adjustment for hazard ratio variation.

PURPOSE: Although single nucleotide polymorphisms (SNPs) of NBS1 have been associated with susceptibility to lung and upper aerodigestive tract (UADT) cancers, their relations to cancer survival and measures of effect are largely unknown. METHODS: Using follow-up data from 611 lung cancer cases and 601 UADT cancer cases from a population-based case-control study in Los Angeles, we prospectively evaluated associations of tobacco smoking and 5 NBS1 SNPs with all-cause mortality. Mortality data were obtained from the Social Security Death Index. We used Cox regression to estimate adjusted hazard ratios (HR) for main effects and ratios of hazard ratios (RHR) derived from product terms to assess hazard ratio variations by each SNP. Bayesian methods were used to account for multiple comparisons. RESULTS: We observed 406 (66 %) deaths in lung cancer cases and 247 (41 %) deaths in UADT cancer cases with median survival of 1.43 and 1.72 years, respectively. Ever tobacco smoking was positively associated with mortality for both cancers. We observed an upward dose-response association between smoking pack-years and mortality in UADT squamous cell carcinoma. The adjusted HR relating smoking to mortality in non-small cell lung cancer (NSCLC) was greater for cases with the GG genotype of NBS1 rs1061302 than for cases with AA/AG genotypes (semi-Bayes adjusted RHR = 1.97; 95 % limits = 1.14, 3.41). CONCLUSIONS: A history of tobacco smoking at cancer diagnosis was associated with mortality among patients with lung cancer or UADT squamous cell carcinoma. The HR relating smoking to mortality appeared to vary with the NBS1 rs1061302 genotype among NSCLC cases.

Single nucleotide polymorphisms of ADH1B, ADH1C and ALDH2 genes and esophageal cancer: a population-based case-control study in China.

Alcohol drinking is a major risk factor for esophageal cancer (EC) and the metabolism of ethanol has been suggested to play an important role in esophageal carcinogenesis. Epidemiologic studies, including genomewide association studies (GWAS), have identified single nucleotide polymorphisms (SNPs) in alcohol dehydrogenases (ADHs) and aldehyde dehydrogenases (ALDHs) to be associated with EC. Using a population-based case-control study with 858 EC cases and 1,081 controls conducted in Jiangsu Province, China, we aimed to provide further information on the association of ADH1B (rs1229984), ADH1C (rs698) and ALDH2 (rs671) polymorphisms with EC in a Chinese population. Results showed that ADH1B (rs1229984) was associated with EC with odds ratios (ORs) of 1.34 [95% confidence interval (CI): 1.08-1.66] for G-allele carriers compared to A/A homozygotes. No heterogeneity was detected on this association across different strata of alcohol drinking and tobacco smoking. Statistical interaction between ALDH2 (rs671) and alcohol drinking on EC susceptibility in both additive and multiplicative scales was observed. Compared to G/G homozygotes, A-allele carriers were positively associated with EC among moderate/heavy drinkers (OR = 1.64, 95% CI: 1.12-2.40) and inversely associated with EC among never/light drinks (OR = 0.75, 95% CI: 0.54-1.03). In addition, statistical interaction between ALDH2 and ADH1B polymorphisms on EC susceptibility among never/light drinkers was indicated. We did not observe association of ADH1C polymorphism with EC. In conclusion, our findings indicated that ADH1B (rs1229984) was associated with EC independent of alcohol drinking and tobacco smoking status and alcohol drinking interacted with ALDH2 (rs671) on EC susceptibility in this high-risk Chinese population.

Indoor air pollution and risk of lung cancer among Chinese female non-smokers.

PURPOSE: To investigate indoor particulate matter (PM) level and various indoor air pollution exposure, and to examine their relationships with risk of lung cancer in an urban Chinese population, with a focus on non-smoking women. METHODS: We conducted a case-control study in Taiyuan, China, consisting of 399 lung cancer cases and 466 controls, of which 164 cases and 218 controls were female non-smokers. Indoor PM concentrations, including PM(1), PM(2.5), PM(7), PM(10), and TSP, were measured using a particle mass monitor. Unconditional logistic regression models were used to calculate odds ratios (ORs) and 95 % confidence intervals after adjusting for age, education, annual income, and smoking. RESULTS: Among non-smoking women, lung cancer was strongly associated with multiple sources of indoor air pollution 10 years ago, including heavy exposure to environmental tobacco smoke at work (aOR = 3.65), high frequency of cooking (aOR = 3.30), and solid fuel usage for cooking (aOR = 4.08) and heating (aOR(coal stove) = 2.00). Housing characteristics related to poor ventilation, including single-story, less window area, no separate kitchen, no ventilator, and rarely having windows open, are associated with lung cancer. Indoor medium PM(2.5) concentration was 68 µg/m(3), and PM(10) was 230 µg/m(3). PM levels in winter are strongly correlated with solid fuel usage for cooking, heating, and ventilators. PM(1) levels in cases are more than 3 times higher than that in controls. Every 10 µg/m(3) increase in PM(1) is associated with 45 % increased risk of lung cancer. CONCLUSIONS: Indoor air pollution plays an important role in the development of lung cancer among non-smoking Chinese women.

Association of XRCC3 and XRCC4 gene polymorphisms, family history of cancer and tobacco smoking with non-small-cell lung cancer in a Chinese population: a case-control study.

Single-nucleotide polymorphisms (SNPs) of DNA repair genes have been reported to modify cancer risk. This study aimed to determine SNPs of the DNA repair genes X-ray repair cross-complementing group 3 (XRCC3) and X-ray cross-complementing group 4 (XRCC4) and their association with non-small-cell lung cancer (NSCLC) susceptibility in a Chinese population. A total of 507 NSCLC patients and 662 healthy controls were recruited for genotyping. Epidemiological and clinical data were also collected for association studies. The data showed that the rs1799794 G allele in the XRCC3 gene and minor allele carriers of XRCC4, including rs1056503 and rs9293337, were inversely associated with NSCLC risk (GG vs homozygote AA), whereas the rs861537 AG or AA genotype and XRCC4 rs6869366 had a significantly increased NSCLC risk. Furthermore, tobacco smoking over 26 pack-years, a family history of lung cancer, exposure to environmental tobacco smoke (ETS) and negative mental status were risk factors for developing NSCLC. This study suggests that SNPs of XRCC3 and XRCC4 and other environmental factors are risk factors for developing NSCLC in this Chinese Han population.

TP53 genetic polymorphisms, interactions with lifestyle factors and lung cancer risk: a case control study in a Chinese population.

BACKGROUND: A pathway-based genotyping analysis suggested rs2078486 was a novel TP53 SNP, but very few studies replicate this association. TP53 rs1042522 is the most commonly studied SNP, but very few studies examined its potential interaction with environmental factors in relation to lung cancer risk. This study aims to examine associations between two TP53 single-nucleotide polymorphisms (SNPs) (rs2078486, rs1042522), their potential interaction with environmental factors and risk of lung cancer. METHODS: A case-control study was conducted in Taiyuan, China. Unconditional logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (95% CIs). Multiplicative and additive interactions between TP53 SNPs and lifestyle factors were evaluated. RESULTS: Variant TP53 rs2078486 SNP was significantly associated with elevated lung cancer risk among smokers (OR: 1.70, 95% CI: 1.08 - 2.67) and individuals with high indoor air pollution exposure (OR: 1.51, 95% CI: 1.00-2.30). Significant or borderline significant multiplicative and additive interactions were found between TP53 rs2078486 polymorphism with smoking and indoor air pollution exposure. The variant genotype of TP53 SNP rs1042522 significantly increased lung cancer risk in the total population (OR: 1.57, 95% CI: 1.11-2.21), but there was no evidence of heterogeneity among individuals with different lifestyle factors. CONCLUSIONS: This study confirmed that TP53 rs2078486 SNP is potentially a novel TP53 SNP that may affect lung cancer risk. Our study also suggested potential synergetic effects of TP53 rs2078486 SNP with smoking and indoor air pollution exposure on lung cancer risk.

Genetic variants of peroxisome proliferator-activated receptor δ are associated with gastric cancer.

BACKGROUND: Peroxisome proliferator-activated receptors (PPAR) are implicated in pathogenesis of insulin resistance and cancers of the digestive system. AIM: We investigated the associations of single nucleotide polymorphisms (SNPs) of PPAR δ and γ with gastric cancer and explored interactions with risk factors of gastric cancer. METHODS: We conducted our analysis in a case-control study of 196 gastric cancer patients and 397 controls residing in the Taixing region of Jiangsu, China. Six SNPs in the PPARδ (rs2076167, rs3734254) and PPARγ genes (rs10865710, rs1801282, rs3856806, rs13306747) were genotyped. We employed logistic regression to evaluate the association between each genotype and gastric cancer and tested for gene-environment interaction with Helicobacter pylori (H. pylori) infection, smoking status, and meat and salt intake. RESULTS: We found that the G/G variant rs2076167, in tight linkage disequilibrium with rs3734254 (R (2) = 0.97), was associated with increased risk of gastric cancer in a recessive model (OR 2.20, 95 % CI 1.12, 4.32). The association between G/G variant of rs2016167 and gastric cancer was particularly strong among those with higher salt intake (OR 5.11, 95 % CI 1.11, 23.5), but did not vary by H. pylori infection or smoking status. CONCLUSION: We found that genetic variants of PPARδ were associated with gastric cancer. If the association is confirmed in larger studies, it may implicate a role for PPARδ activators, such as insulin-sensitizing agents, in prevention of gastric cancer.

Hospital-level variation in racial disparities in low-risk nulliparous cesarean delivery rates.

BACKGROUND: Nationally, rates of cesarean delivery are highest among Black patients compared with other racial/ethnic groups. These observed inequities are a relatively new phenomenon (in the 1980s, cesarean delivery rates among Black patients were lower than average), indicating an opportunity to narrow the gap. Cesarean delivery rates vary greatly among hospitals, masking racial disparities that are unseen when rates are reported in aggregate. OBJECTIVE: This study aimed to explore reasons for the current large Black-White disparity in first-birth cesarean delivery rates by first examining the hospital-level variation in first-birth cesarean delivery rates among different racial/ethnic groups. We then identified hospitals that had low first-birth cesarean delivery rates among Black patients and compared them with hospitals with high rates. We sought to identify differences in facility or patient characteristics that could explain the racial disparity. STUDY DESIGN: A population cross-sectional study was performed on 1,267,493 California live births from 2018 through 2020 using birth certificate data linked with maternal patient discharge records. Annual nulliparous term singleton vertex cesarean delivery (first-birth) rates were calculated for the most common racial/ethnic groups statewide and for each hospital. Self-identified race/ethnicity categories as selected on the birth certificate were used. Relative risk and 95% confidence intervals for first-birth cesarean delivery comparing 2019 with 2015 were estimated using a log-binomial model for each racial/ethnic group. Patient and hospital characteristics were compared between hospitals with first-birth cesarean delivery rates <23.9% for Black patients and hospitals with rates ≥23.9% for Black patients. RESULTS: Hospitals with at least 30 nulliparous term singleton vertex Asian, Black, Hispanic, and White patients each were identified. Black patients had a very different distribution, with a significantly higher rate (28.4%) and wider standard deviation (7.1) and interquartile range (6.5) than other racial groups (P<.01). A total of 29 hospitals with a low first-birth cesarean delivery rate among Black patients were identified using the Healthy People 2020 target of 23.9% and compared with 106 hospitals with higher rates. The low-rate group had a cesarean delivery rate of 19.9%, as opposed to 30.7% in the higher-rate group. There were no significant differences between the groups in hospital characteristics (ownership, delivery volume, neonatal level of care, proportion of midwife deliveries) or patient characteristics (age, education, insurance, onset of prenatal care, body mass index, hypertension, diabetes mellitus). Among the 106 hospitals that did not meet the target for Black patients, 63 met it for White patients with a mean rate of 21.4%. In the same hospitals, the mean rate for Black patients was 29.5%. Among Black patients in the group that did not meet the 23.9% target, there were significantly higher rates of all cesarean delivery indications: labor dystocia, fetal concern (spontaneous labor), and no labor (eg, macrosomia), which are all indications with a high degree of subjectivity. CONCLUSION: The statewide cesarean delivery rate of Black patients is significantly higher and has substantially greater hospital variation compared with other racial or ethnic groups. The lack of difference in facility or patient characteristics between hospitals with low cesarean delivery rates among Black patients and those with high rates suggests that unconscious bias and structural racism potentially play important roles in creating these racial differences.