We examined prospectively risk factors which might contribute to INH-induced liver damage in 113 patients taking preventive INH for at least 8 weeks. Twelve who had abnormal initial liver tests did not get worse with INH, while 19/101 with normal initial tests developed significant liver dysfunction, mostly hepatocellular, three having overt hepatitis. When 12 other patients who drank alcohol were excluded from analysis, there were still 15/89 with significant liver dysfunction, 12 of whom were slow acetylators (p<0.05). The only other risk factor was age. By combining acetylator phenotype with age, but excluding alcohol, we calculated the risk of INH-induced liver enzyme elevation as follows: under 35 years—fast acetylators, 3.7%, slow acetylators, 13%; over 35—fast acetylators, 13.2%, slow acetylators, 37% (p <0.02). Fast acetylation is thus not a risk factor for developing INH-induced liver dysfunction; indeed, the contrary seems to be the case.