The relationship of anemia as a risk factor for maternal mortality was analyzed by using cross-sectional, longitudinal and case-control studies because randomized trials were not available for analysis. The following six methods of estimation of mortality risk were adopted: 1) the correlation of maternal mortality rates with maternal anemia prevalence derived from national statistics; 2) the proportion of maternal deaths attributable to anemia; 3) the proportion of anemic women who die; 4) population-attributable risk of maternal mortality due to anemia; 5) adolescence as a risk factor for anemia-related mortality; and 6) causes of anemia associated with maternal mortality. The average estimates for all-cause anemia attributable mortality (both direct and indirect) were 6.37, 7.26 and 3.0% for Africa, Asia and Latin America, respectively. Case fatality rates, mainly for hospital studies, varied from <1% to >50%. The relative risk of mortality associated with moderate anemia (hemoglobin 40-80 g/L) was 1.35 [95% confidence interval (CI): 0.92-2.00] and for severe anemia (<47 g/L) was 3.51 (95% CI: 2.05-6.00). Population-attributable risk estimates can be defended on the basis of the strong association between severe anemia and maternal mortality but not for mild or moderate anemia. In holoendemic malarious areas with a 5% severe anemia prevalence (hemoglobin <70 g/L), it was estimated that in primigravidae, there would be 9 severe-malaria anemia-related deaths and 41 nonmalarial anemia-related deaths (mostly nutritional) per 100,000 live births. The iron deficiency component of these is unknown.

The relationship of anemia as a risk factor for child mortality was analyzed by using cross-sectional, longitudinal and case-control studies, and randomized trials. Five methods of estimation were adopted: 1) the proportion of child deaths attributable to anemia; 2) the proportion of anemic children who die in hospital studies; 3) the population-attributable risk of child mortality due to anemia; 4) survival analyses of mortality in anemic children; and 5) cause-specific anemia-related child mortality. Most of the data available were hospital based. For children aged 0-5 y the percentage of deaths due to anemia was comparable for reports from highly malarious areas in Africa (Sierra Leone 11.2%, Zaire 12.2%, Kenya 14.3%). Ten values available for hemoglobin values <50 g/L showed a variation in case fatality from 2 to 29.3%. The data suggested little if any dose-response relating increasing hemoglobin level (whether by mean value or selected cut-off values) with decreasing mortality. Although mortality was increased in anemic children with hemoglobin <50 g/L, the evidence for increased risk with less severe anemia was inconclusive. The wide variation for mortality with hemoglobin <50 g/L is related to methodological variation and places severe limits on causal inference; in view of this, it is premature to generate projections on population-attributable risk. A preliminary survival analysis of an infant cohort from Malawi indicated that if the hemoglobin decreases by 10 g/L at age 6 mo, the risk of dying becomes 1.72 times higher. Evidence from a number of studies suggests that mortality due to malarial severe anemia is greater than that due to iron-deficiency anemia. Data are scarce on anemia and child mortality from non-malarious regions. Primary prevention of iron-deficiency anemia and malaria in young children could have substantive effects on reducing child mortality from severe anemia in children living in malarious areas.

The proportion of blood meals taken on humans which are infectious to mosquitoes in the Madang area, Papua New Guinea was estimated by two methods. In the first, laboratory reared Anopheles farauti were fed on individuals of all ages at village surveys. The results showed that 3.8% of people were infectious and that the mean percentage of mosquitoes which became infected by feeding on these people was 37.9%. From the average proportion of mosquitoes infected, the probability that a mosquito feeding on a human would pick up infection was 0.013 +/- 0.005. In the second approach mosquitoes were fed on identified Plasmodium falciparum, P. vivax and P. malariae gametocyte carriers. The results indicated that 46% of gametocyte carriers were infectious and that the mean probability of a mosquito becoming infected after feeding on a gametocyte carrier was 0.151 +/- 0.029. Gametocyte prevalence rates in all ages measured over 18 months in three villages averaged 3.3% P. falciparum, 4.0% P. vivax and 0.7% P. malariae, totalling 8.0 +/- 0.7%. Combining gametocyte prevalence rates with the probability of a mosquito becoming infected from a gametocyte carrier, the probability of a mosquito becoming infected following a blood meal on a member of the human population was estimated to be 0.012 +/- 0.003.