Estimated seroprevalence of SARS-CoV-2 antibodies among adults in Orange County, California.

Clinic-based estimates of SARS-CoV-2 may considerably underestimate the total number of infections. Access to testing in the US has been heterogeneous and symptoms vary widely in infected persons. Public health surveillance efforts and metrics are therefore hampered by underreporting. We set out to provide a minimally biased estimate of SARS-CoV-2 seroprevalence among adults for a large and diverse county (Orange County, CA, population 3.2 million). We implemented a surveillance study that minimizes response bias by recruiting adults to answer a survey without knowledge of later being offered SARS-CoV-2 test. Several methodologies were used to retrieve a population-representative sample. Participants (n = 2979) visited one of 11 drive-thru test sites from July 10th to August 16th, 2020 (or received an in-home visit) to provide a finger pin-prick sample. We applied a robust SARS-CoV-2 Antigen Microarray technology, which has superior measurement validity relative to FDA-approved tests. Participants include a broad age, gender, racial/ethnic, and income representation. Adjusted seroprevalence of SARS-CoV-2 infection was 11.5% (95% CI: 10.5-12.4%). Formal bias analyses produced similar results. Prevalence was elevated among Hispanics (vs. other non-Hispanic: prevalence ratio [PR] = 1.47, 95% CI 1.22-1.78) and household income < $50,000 (vs. > $100,000: PR = 1.42, 95% CI: 1.14 to 1.79). Results from a diverse population using a highly specific and sensitive microarray indicate a SARS-CoV-2 seroprevalence of ~ 12 percent. This population-based seroprevalence is seven-fold greater than that using official County statistics. In this region, SARS-CoV-2 also disproportionately affects Hispanic and low-income adults.

Subacute sclerosing panencephalitis mortality, United States, 1979-2016: Vaccine-induced declines in SSPE deaths.

Subacute sclerosing panencephalitis (SSPE) is a neurodegenerative disease caused by measles virus. We estimate SSPE age-specific mortality in the United States, 1979-2016. The general decline in SSPE mortality reflects that of measles. Shifts, over time, in SSPE mortality by age echo changes in the age distribution of measles in the 1970s and in the 1989-91 outbreak. The current epidemiological situation is that autochthonous SSPE will disappear in the United States, assuming measles vaccination rates remain high.

"You've Come a Long Way, Baby": The Convergence in Age Patterns of Lung Cancer Mortality by Sex, United States, 1959-2013.

We analyze lung cancer mortality by age and sex in the United States, 1959-2013. It is already known that male lung cancer death rates exceed those of women and that tobacco use is the leading reason for the sex difference. We elaborate on this knowledge by showing that unlike most causes of death, lung cancer mortality patterns by age are a very good fit to a quadratic-Gompertz model, i.e., log mortality rates are quadratic by age, with the mode above age 70. With a little additional historical data on sex differences in tobacco use, the quadratic models help to paint a clear quantitative picture of behavior-led convergence in lung cancer mortality by sex. The shape of the sex-specific mortality curves have converged dramatically: since 1983, the sexes have had statistically indistinguishable shapes of their quadratic-Gompertz mortality curves. Female lung cancer mortality patterns have shown a transformation from a nonsmoking to a smoking pattern. The modal age of the quadratic-Gompertzian lung cancer death rates has potential application in countries at earlier stages of the global tobacco epidemic. Where the modal age is falling (year-on-year), we can infer that the local lung cancer epidemic is getting worse, and where it is rising, that it has begun to abate.

Did the 1918 influenza cause the twentieth century cardiovascular mortality epidemic in the United States?

During most of the twentieth century, cardiovascular mortality increased in the United States while other causes of death declined. By 1958, the age-standardized death rate (ASDR) for cardiovascular causes for females was 1.84 times that for all other causes, combined (and, for males, 1.79×). Although contemporary observers believed that cardiovascular mortality would remain high, the late 1950s and early 1960s turned out to be the peak of a roughly 70-year epidemic. By 1988 for females (1986 for males), a spectacular decline had occurred, wherein the ASDR for cardiovascular causes was less than that for other causes combined. We discuss this phenomenon from a demographic point of view. We also test a hypothesis from the literature, that the 1918 influenza pandemic caused the cardiovascular mortality epidemic; we fail to find support.

A 'post-honeymoon' measles epidemic in Burundi: mathematical model-based analysis and implications for vaccination timing.

Using a mathematical model with realistic demography, we analyze a large outbreak of measles in Muyinga sector in rural Burundi in 1988-1989. We generate simulated epidemic curves and age × time epidemic surfaces, which we qualitatively and quantitatively compare with the data. Our findings suggest that supplementary immunization activities (SIAs) should be used in places where routine vaccination cannot keep up with the increasing numbers of susceptible individuals resulting from population growth or from logistical problems such as cold chain maintenance. We use the model to characterize the relationship between SIA frequency and SIA age range necessary to suppress measles outbreaks. If SIAs are less frequent, they must expand their target age range.

Clostridium difficile Infection: An Emerging Cause of Death in the Twenty-First Century.

Enterocolitis due to Clostridium difficile is major emerging cause of death in the U.S. Between 1999 and 2012, C. diff. deaths rose by a staggering almost ten-fold amount, to 7,739 from 793. This article has three goals. First, we present a demographic description of C. diff. mortality in the U.S. since 1999. Second, we test a hypothesis that the increase in C. diff. deaths is due to population aging. We find that the emergence of this cause of death follows a proportional hazard pattern above age 40. Thus, population aging is not the only factor responsible for the increase in C. diff. deaths. This, combined with a contributory cause of death analysis, points towards health care-based strategies to combat C. diff. Third, we demonstrate a simple weighted least squares technique for estimating Gompertz models that gives parameter estimates that are closer to full maximum likelihood than conventional approaches.

Assessing the direct effects of the ebola outbreak on life expectancy in liberia, sierra leone and Guinea.

BACKGROUND: An EVD outbreak may reduce life expectancy directly (due to high mortality among EVD cases) and indirectly (e.g., due to lower utilization of healthcare and subsequent increases in non-EVD mortality). In this paper, we investigated the direct effects of EVD on life expectancy in Liberia, Sierra Leone and Guinea (LSLG thereafter). METHODS: We used data on EVD cases and deaths published in situation reports by the World Health Organization (WHO), as well as data on the age of EVD cases reported from patient datasets. We used data on non-EVD mortality from the most recent life tables published prior to the EVD outbreak. We then formulated three scenarios based on hypotheses about a) the extent of under-reporting of EVD cases and b) the EVD case fatality ratio. For each scenario, we re-estimated the number of EVD deaths in LSLG and we applied standard life table techniques to calculate life expectancy. RESULTS: In Liberia, possible reductions in life expectancy resulting from EVD deaths ranged from 1.63 year (low EVD scenario) to 5.56 years (high EVD scenario), whereas in Sierra Leone, possible life expectancy declines ranged from 1.38 to 5.10 years. In Guinea, the direct effects of EVD on life expectancy were more limited (<1.20 year). CONCLUSIONS: Our high EVD scenario suggests that, due to EVD deaths, life expectancy may have declined in Liberia and Sierra Leone to levels these two countries had not experienced since 2001-2003, i.e., approximately the end of their civil wars. The total effects of EVD on life expectancy may however be larger due to possible concomitant increases in non-EVD mortality during the outbreak.

Influenza as a proportion of pneumonia mortality: United States, 1959-2009.

As causes of death, influenza and pneumonia are typically analyzed together. We quantify influenza's contribution to the combined pneumonia and influenza mortality time series for the United States, 1959-2009. A key statistic is I/(P + I), the proportion of pneumonia and influenza mortality accounted for by influenza. Year-to-year, I/(P + I) is highly variable and shows long-term decline. Extreme values of I/(P + I) are associated with extreme P + I death rates and vice versa, but I/(P + I) is a weak predictor of P + I mortality overall. Prominence of influenza in the medical news is associated with high I/(P + I). Influenza and pneumonia should be analyzed as a combined cause.

Vitamin D (25OHD) Serum Seasonality in the United States.

BACKGROUND: Vitamin D is an important micronutrient for health. Hypovitaminosis D is thought to play a role in the seasonality of a number of diseases and adverse health conditions. To refine hypotheses about the links between vitamin D and seasonal diseases, good estimates of the cyclicality of serum vitamin D are necessary. OBJECTIVES: The objective of this study is to describe quantitatively the cyclicality of 25-hydroxyvitamin D (25OHD) in the United States. We provide a statistical analysis with weekly time resolution, in comparison to the quarterly (winter/spring/summer/fall) estimates already in the literature. METHODS: We analyzed time series data on 25OHD, spanning 287 consecutive weeks. The pooled data set comes from 3.44 million serum samples from the United States. We statistically analyzed the proportion of sera that were vitamin D sufficient, defined as 25OHD [Formula: see text] ng/mL, as a function of date. RESULTS: In the United States, serum 25OHD follows a lagged pattern relative to the astronomical seasons, peaking in late summer (August) and troughing in late winter (February). Airmass, which is a function of solar altitude, fits the 25OHD data very well when lagged by 8 weeks. CONCLUSIONS: Serum vitamin D levels can be modeled as a function of date, working through a double-log transformation of minimal solar airmass (easily calculated from solar altitude, retrievable from an online solar altitude/azimuth table).

Influenza mortality in the United States, 2009 pandemic: burden, timing and age distribution.

BACKGROUND: In April 2009, the most recent pandemic of influenza A began. We present the first estimates of pandemic mortality based on the newly-released final data on deaths in 2009 and 2010 in the United States. METHODS: We obtained data on influenza and pneumonia deaths from the National Center for Health Statistics (NCHS). Age- and sex-specific death rates, and age-standardized death rates, were calculated. Using negative binomial Serfling-type methods, excess mortality was calculated separately by sex and age groups. RESULTS: In many age groups, observed pneumonia and influenza cause-specific mortality rates in October and November 2009 broke month-specific records since 1959 when the current series of detailed US mortality data began. Compared to the typical pattern of seasonal flu deaths, the 2009 pandemic age-specific mortality, as well as influenza-attributable (excess) mortality, skewed much younger. We estimate 2,634 excess pneumonia and influenza deaths in 2009-10; the excess death rate in 2009 was 0.79 per 100,000. CONCLUSIONS: Pandemic influenza mortality skews younger than seasonal influenza. This can be explained by a protective effect due to antigenic cycling. When older cohorts have been previously exposed to a similar antigen, immune memory results in lower death rates at older ages. Age-targeted vaccination of younger people should be considered in future pandemics.

Immigrant health around the world: evidence from the World Values Survey.

We describe the relationship between immigrant status and self-rated health around the world, both in raw descriptive statistics and in models controlling for individual characteristics. Using the World Values Survey (1981-2005), we analyze data from 32 different countries worldwide. We estimate four regression models per country. The basic model tests mean differences in self-rated health. Additional models add demographic and social class controls. Introduction of control variables (most particularly, age) changes the results dramatically. In the final model, net of controls, only two countries show poorer immigrant health and three countries show better immigrant health. The multivariate regression models net of controls show few differences in health status between immigrants and the native born. The age structure of immigrant populations is an important mediator of differences in health status compared to the native-born population.

The 1918 influenza pandemic hastened the decline of tuberculosis in the United States: an age, period, cohort analysis.

The effect of the 1918 influenza pandemic on other diseases is a neglected topic in historical epidemiology. This paper takes up the hypothesis that the influenza pandemic affected the long-term decline of tuberculosis through selective mortality, such that many people with tuberculosis were killed in 1918, depressing subsequent tuberculosis mortality and transmission. Regularly collected vital statistics data on mortality of influenza and tuberculosis in the US are presented and analyzed demographically. The available population-level data fail to contradict the selection hypothesis. More work is needed to understand fully the role of multiple morbidities in the 1918 influenza pandemic.

Cause of death affects racial classification on death certificates.

Recent research suggests racial classification is responsive to social stereotypes, but how this affects racial classification in national vital statistics is unknown. This study examines whether cause of death influences racial classification on death certificates. We analyze the racial classifications from a nationally representative sample of death certificates and subsequent interviews with the decedents' next of kin and find notable discrepancies between the two racial classifications by cause of death. Cirrhosis decedents are more likely to be recorded as American Indian on their death certificates, and homicide victims are more likely to be recorded as Black; these results remain net of controls for followback survey racial classification, indicating that the relationship we reveal is not simply a restatement of the fact that these causes of death are more prevalent among certain groups. Our findings suggest that seemingly non-racial characteristics, such as cause of death, affect how people are racially perceived by others and thus shape U.S. official statistics.