ABSTRACT
INTRODUCTION: Smoking commercial tobacco products is highly prevalent in American Indian and Alaska Native (Indigenous) pregnancies. This disparity directly contributes to maternal and fetal mortality. Our objective was to describe cigarette smoking prevalence, cessation intervention uptake, and cessation behaviors of pregnant Indigenous people compared to sex and age-matched regional cohort. AIMS AND METHODS: Pregnancies from an Indigenous cohort in Olmsted County, Minnesota, identified in the Rochester Epidemiology Project, were compared to pregnancies identified in a sex and age-matched non-Indigenous cohort from 2006 to 2019. Smoking status was defined as current, former, or never. All pregnancies were reviewed to identify cessation interventions and cessation events. The primary outcome was smoking prevalence during pregnancy, with secondary outcomes measuring uptake of smoking cessation interventions and cessation. RESULTS: The Indigenous cohort included 57 people with 81 pregnancies, compared to 226 non-Indigenous people with 358 pregnancies. Smoking was identified during 45.7% of Indigenous pregnancies versus 11.2% of non-Indigenous pregnancies (RR: 3.25, 95% CI = 1.98-5.31, p ≤ .0001). Although there was no difference in uptake of cessation interventions between cohorts, smoking cessation was significantly less likely during Indigenous pregnancies compared to non-Indigenous pregnancies (OR: 0.23, 95% CI = 0.07-0.72, pâ =â .012). CONCLUSIONS: Indigenous pregnant people in Olmsted County, Minnesota were more than three times as likely to smoke cigarettes during pregnancy compared to the non-indigenous cohort. Despite equivalent uptake of cessation interventions, Indigenous people were less likely to quit than non-Indigenous people. Understanding why conventional smoking cessation interventions were ineffective at promoting cessation during pregnancy among Indigenous women warrants further study. IMPLICATIONS: Indigenous pregnant people in Olmsted County, Minnesota, were greater than three times more likely to smoke during pregnancy compared to a regional age matched non-Indigenous cohort. Although Indigenous and non-Indigenous pregnant people had equivalent uptake of cessation interventions offered during pregnancy, Indigenous people were significantly less likely to quit smoking before fetal delivery. This disparity in the effectiveness of standard of care interventions highlights the need for further study to understand barriers to cessation in pregnant Indigenous people.
Subject(s)
American Indian or Alaska Native , Cigarette Smoking , Smoking Cessation , Female , Humans , Pregnancy , American Indian or Alaska Native/statistics & numerical data , Cigarette Smoking/epidemiology , Cigarette Smoking/ethnology , Prenatal Care , Smoking Cessation/statistics & numerical data , Minnesota/epidemiology , PrevalenceABSTRACT
OBJECTIVE: To describe smoking behaviors and pharmaceutical cessation aid uptake in a population-based Indigenous cohort compared with an age- and sex-matched non-Indigenous cohort. PATIENTS AND METHODS: Using the health record-linkage system of the Rochester Epidemiology Project (January 1, 2006, to December 31, 2019), smoking data of Indigenous residents of Olmsted County in Minnesota were abstracted to define the smoking prevalence, incidence, cessation, relapse after cessation, and pharmaceutical smoking cessation aid uptake compared with a matched non-Indigenous cohort. Prevalence was analyzed with a modified Poisson regression; cessation and relapse were evaluated with generalized estimating equations. Incidence was evaluated with a Cox proportional hazards model. RESULTS: Smoking prevalence was higher in the Indigenous cohort (39.0% to 47.0%; n=898) than the matched cohort (25.6% to 30.3%; n=1780). Pharmaceutical uptake was higher among the Indigenous cohort (35.8% of n=584 ever smokers vs 16.3% of n=778 ever smokers; P<.001). Smoking cessation events occurred more frequently in the Indigenous cohort (relative risk, 1.10; 95% CI, 1.06 to 1.13; P<.001). Indigenous former smokers were more likely to resume smoking (relative risk, 3.03; 95% CI, 2.93 to 3.14; P<.001) compared with the matched cohort. These findings were independent of socioeconomic status, age, and sex. CONCLUSION: Smoking in this Indigenous cohort was more prevalent compared with a sex- and age-matched non-Indigenous cohort despite more smoking cessation events and higher use of smoking cessation aids in the Indigenous cohort. The relapse rate after achieving cessation in the Indigenous cohort was more than three times higher than the non-Indigenous cohort. This finding has not been previously described and represents a potential target for relapse prevention efforts in US Indigenous populations.
Subject(s)
Smoking Cessation , Smoking , Humans , Minnesota/epidemiology , Pharmaceutical Preparations , Recurrence , Smoking/epidemiologyABSTRACT
OBJECTIVE: To investigate an association between tumor necrosis factors-alpha (TNFα) inhibitors or other immunosuppressants and the development of uveal and cutaneous melanoma. PATIENTS AND METHODS: We performed a retrospective incidence and case-control analysis of patients in Olmsted County, MN, who were diagnosed with uveal or cutaneous melanoma from January 1, 2000, to December 31, 2014. Incidence was adjusted by age and gender to the 2010 US white population. Controls were matched by sex and age to cases at time of diagnosis of melanoma. RESULTS: There were 1221 cases of melanoma (33 uveal, 1188 cutaneous). Combined incidence of uveal and cutaneous melanoma per 100,000 person-years varied by gender (male > female), age (older > younger), and time period: 2010 to 2014 (77.9, 95% confidence interval [CI], 71.1-84.7) ≈ 2005 to 2009 (78.0, 95% CI, 70.9-85.0) > 2000 to 2004 (42.5, 95% CI, 36.9-48.1, P<.001). TNFa inhibitor prescription was not associated with significantly increased risk of melanoma vs controls (1.06% vs 0.41%, P=.06). Immunosuppressive agents, high-dose corticosteroids, and topical immunosuppressants were associated with melanoma (odds ratio [OR] 1.42 CI, 1.03-1.95, 3.30 CI, 2.44-4.48, and 1.87 CI, 1.06-3.28, respectively). An increased number of patients with uveal melanoma received immune modulating agents vs controls, but this was not statistically significant (P=.36). Autoimmune disease itself was not correlated with melanoma (P=.73). CONCLUSION: Exposure to immunosuppressive agents is associated with melanoma. TNFa inhibition and autoimmune disease alone do not significantly increase risk of melanoma. In patients receiving immunosuppressive treatments, physicians should consider monitoring with dilated ophthalmic and full-body skin examinations. Further studies are needed to assess the impact of TNFa inhibitors on development of melanoma, particularly in uveal melanoma.
Subject(s)
Immunosuppressive Agents/adverse effects , Melanoma/chemically induced , Skin Neoplasms/chemically induced , Tumor Necrosis Factor-alpha/adverse effects , Uveal Neoplasms/chemically induced , Aged , Aged, 80 and over , Case-Control Studies , Female , Humans , Incidence , Male , Melanoma/epidemiology , Melanoma/pathology , Middle Aged , Minnesota/epidemiology , Retrospective Studies , Risk Factors , Skin Neoplasms/epidemiology , Skin Neoplasms/pathology , Tumor Necrosis Factor-alpha/antagonists & inhibitors , Tumor Necrosis Factor-alpha/therapeutic use , Uveal Neoplasms/epidemiology , Uveal Neoplasms/pathology , Melanoma, Cutaneous MalignantABSTRACT
OBJECTIVE: To examine an association between melanoma and Parkinson disease (PD). PATIENTS AND METHODS: Phase I: Rochester Epidemiology Project records were used to identify (between January 1, 1976, and December 31, 2013) patients with PD in Olmsted County, Minnesota, with 3 matched controls per case. After review, JMP statistical software with logistic regression analysis was used to assess the risk of preexisting melanoma in patients with PD vs controls. Phase II: All Rochester Epidemiology Project cases of melanoma were identified (between January 1, 1976, and December 31, 2014), with 1 control per case. A Cox proportional hazards model was used to assess the risk of developing PD after the index date in cases vs controls, and Kaplan-Meier analysis was performed to determine the 35-year cumulative risk of PD. A Cox proportional hazards model was used to assess the risk of death from metastatic melanoma in patients with melanoma without PD compared with those with PD. RESULTS: Phase I: Patients with PD had a 3.8-fold increased likelihood of having preexisting melanoma as compared with controls (95% CI, 2.1-6.8; P<.001). Phase II: Patients with melanoma had a 4.2-fold increased risk of developing PD (95% CI, 2.0-8.8; P<.001). Kaplan-Meier analysis revealed an increased 35-year cumulative risk of PD in patients with melanoma (11.8%) compared with controls (2.6%) (P<.001). Patients with melanoma without PD had a 10.5-fold increased relative risk of death from metastatic melanoma compared with patients with melanoma with PD (95% CI, 1.5-72.2) (P=.02). CONCLUSION: There appears to be an association between melanoma and PD. Further study is warranted; but on the basis of these results, physicians may consider counseling patients with melanoma about PD risk and implementing cutaneous and ocular melanoma surveillance in patients with PD.