There are no studies of oral health in relation to esophageal cancer in Africa, or of Eastern Africa's endemic dental fluorosis, an irreversible enamel hypo‐mineralization due to early‐life excessive fluoride intake. During 2014–18, we conducted a case–control study of squamous cell esophageal cancer in Eldoret, western Kenya. Odds ratios (AORs (95% confidence intervals)) were adjusted for design factors, tobacco, alcohol, ethnicity, education, oral hygiene and missing/decayed teeth. Esophageal cancer cases (N = 430) had poorer oral health and hygiene than controls (N = 440). Compared to no dental fluorosis, moderate/severe fluorosis, which affected 44% of cases, had a crude OR of 20.8 (11.6, 37.4) and on full adjustment was associated with 9.4‐fold (4.6, 19.1) increased risk, whilst mild fluorosis (43% of cases) had an AOR of 2.3 (1.3, 4.0). The prevalence of oral leukoplakia and tooth loss/decay increased with fluorosis severity, and increased cancer risks associated with moderate/severe fluorosis were particularly strong in individuals with more tooth loss/decay. Using a mswaki stick (AOR = 1.7 (1.0, 2.9)) rather than a commercial tooth brush and infrequent tooth brushing also independently increased risk. Geographic variations showed that areas of high esophageal cancer incidence and those of high groundwater fluoride levels have remarkably similar locations across Eastern Africa. In conclusion, poor oral health in combination with, or as a result of, high‐altitude susceptibility to hydro‐geologically influenced dental fluorosis may underlie the striking co‐location of Africa's esophageal cancer corridor with the Rift Valley. The findings call for heightened research into primary prevention opportunities of this highly fatal but common cancer.

Squamous cell esophageal cancer is common throughout East Africa, but its etiology is poorly understood. We investigated the contribution of alcohol consumption to esophageal cancer in Kenya, based on a hospital-based case-control study conducted from 08/2013 to 03/2018 in Eldoret, western Kenya. Cases had an endoscopy-confirmed esophageal tumor whose histology did not rule out squamous cell carcinoma. Age and gender frequency-matched controls were recruited from hospital visitors/patients without digestive diseases. Logistic regression was used to calculate odds ratios (ORs) and their 95% confidence intervals (CI) adjusting for tobacco (type, intensity) and 6 other potential confounders. A total of 422 cases (65% male, mean at diagnosis 60 (SD 14) years) and 414 controls were included. ORs for ever-drinking were stronger in ever-tobacco users (9.0, 95% CI: 3.4, 23.8, with few tobacco users who were never drinkers) than in never-tobacco users (2.6, 95% CI: 1.6, 4.1). Risk increased linearly with number of drinks: OR for >6 compared to >0 to ≤2 drinks/day were 5.2 (2.4, 11.4) in ever-tobacco users and 2.1 (0.7, 4.4) in never-tobacco users. Although most ethanol came from low ethanol alcohols (busaa or beer), for the same ethanol intake, if a greater proportion came from the moonshine chang'aa, it was associated with a specific additional risk. The population attributable fraction for >2 drinks per day was 48% overall and highest in male tobacco users. Alcohol consumption, particularly of busaa and chang'aa, contributes to half of the esophageal cancer burden in western Kenya.

Oesophageal squamous cell carcinoma (ESCC) has markedly high incidence rates in Kenya and much of East Africa, with a dire prognosis and poorly understood aetiology. Consumption of hot beverages—a probable carcinogen to humans—is associated with increased ESCC risk in other settings and is habitually practiced in Kenya. We conducted a case–control study in Eldoret, western Kenya between August 2013 and March 2018. Cases were patients with endoscopically confirmed oesophageal cancer whose histology did not rule out ESCC. Age and sex‐matched controls were hospital visitors and hospital out and in‐patients excluding those with digestive diseases. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated for self‐reported drinking temperatures; consumption frequency; mouth burning frequency and hot porridge consumption using logistic regression models adjusted for potential confounders. Drinking temperature association with tumour sub‐location was also investigated. The study included 430 cases and 440 controls. Drinkers of ‘very hot’ and ‘hot’ beverages (>95% tea) had a 3.7 (95% CI: 2.1–6.5) and 1.4‐fold (1.0–2.0) ESCC risk, respectively compared to ‘warm’ drinkers. This trend was consistent in males, females, never and ever alcohol/tobacco and was stronger over than under age 50 years. The tumour sub‐location distribution (upper/middle/lower oesophagus) did not differ by reported drinking temperature. Our study is the first comprehensive investigation in this setting to‐date to observe a link between hot beverage consumption and ESCC in East Africa. These findings provide further evidence for the role of this potentially modifiable risk factor in ESCC aetiology.

Background The contribution of alcohol to the large burden of oesophageal squamous cell carcinoma (ESCC) in east Africa remains uncertain and difficult to assess owing to complex consumption patterns of traditional and commercial drinks. We aimed to assess whether alcohol drinking, overall and at specific intake levels, contributes to ESCC risk in east Africa. MethodsWe did a hospital-based case-control study in Kenya, Tanzania, and Malawi, which included comprehensive assessment of a variety of locally consumed alcohol that we used to classify drinkers as exclusively low alcohol-byvolume (ABV; <30% ABV) drinkers or drinkers of some high-ABV drinks, as well as the number of drinks consumed, average weekly ethanol intake, and the contribution of each drink type to overall ethanol consumption. Cases were patients aged 18 years and older with incident primary ESCC, confirmed histologically for the majority of cases, and a clinical diagnosis for the remainder. Controls were frequency-matched on age and sex in a 1:1 ratio with cases. The controls were recruited from the same hospitals as cases and included outpatients, inpatients, and hospital visitors who did not have cancer or any other digestive disease. Consenting participants took part in face-to-face interviews in which they were asked whether they had ever consumed alcohol (the primary exposure variable); those who had were asked follow-up questions about their consumption habits for different alcoholic drinks. Findings 1279 cases and 1346 controls were recruited between Aug 5, 2013, and May 24, 2020, including 430 cases and 440 controls from Kenya, 310 cases and 313 controls from Tanzania, and 539 cases and 593 controls from Malawi. 65 (4•8%) of 1344 cases were excluded. Consistent positive associations with ESCC risk were found for ever having consumed alcohol in Kenyan men and Tanzanian men, and for daily number of drinks and estimated ethanol intake in Kenya, Tanzania (both sexes) and Malawian women. Corresponding population-attributable fractions of ESCC for those reporting ever drinking alcohol (vs never drinking) were 65% (95% CI 52-78) in Kenyan men and 23% (<1-45) in Kenyan women, and 56% (95% CI 36-76) in Tanzanian men and 5% (0-42) in Tanzanian women. Increased risk and population-attributable fractions were almost entirely due to risks in high-ABV drinkers.Interpretation Alcohol appears to be a substantial contributor to ESCC risk in east Africa, particularly among men, and a large fraction of ESCC could be prevented by cessation or reduction of alcohol consumption. Future studies should consider independent ascertainment of alcohol intake to assess the potential of under-reporting in Malawi.

Background: Case-control studies remain an important study design for aetiologic research on cancer, particularly when cohorts are not available. In addition to the potential biases inherent in this design, conducting fieldwork in settings with weak health care and information systems for cancer, such as in sub Saharan Africa, confer additional challenges which we present here with the aim to share experience to guide future studies. Methods: We undertook a hospital-based case-control study of squamous cell esophageal cancer at the Moi Teaching and Referral Hospital in Eldoret, West Kenya. Cases were recruited at endoscopy and controls from hospital wards, age and gender frequency-matched to cases. Urine, toenails, blood and tumour biopsy were collected and a questionnaire administered. Results: During this pilot phase, 143 cases and 155 controls were successfully recruited. Complete questionnaire data was obtained through e-data collection. Biospecimen collection was possible with support of an already existing equipped laboratory. We introduce changes made in the main study phase, including on expansion of the control groups to allow to consideration of selection bias. Conclusions: Extra attention and funding to train and monitor data quality and biospecimen collection and reimbursement of a large group held together by strong leadership are essential. We recommend studies based on regional treatment centres with their more defined catchment areas rather than in the capital cities as referral routes in multi-level health care systems are severely attrition prone.