They're a food quality health concern if food is badly contaminated. Even if not badly contaminated, the science, technology and the law still has a way to go before telling the entire story and reducing our exposure to them to safer levels. On a practical level, all you can really do is keep a clean house, live in a developed country and ask companies you buy food from if they carry out testing on any raw materials they use to make or supply food products to you as a consumer.
Major coffee producers will respond to inquiries about mycotoxin levels since they're tested regularly.
For some science, see Mycotoxins: Occurrence, toxicology, and exposure assessment for a good review, which includes a decent non-exhaustive list of types, toxicity and some monitoring information for their occurrence.
The review shows their presence in nuts, dried food, cereals, spices, baby foods, coffee, beer, wine, cocoa, meat, pasta, bread, vegetable oil, juice, cider. Pretty damn near unavoidable, but it looks like lesser developed countries have higher amounts of contamination.
As for harm, the International Agency for Research on Cancer has classified different Mycotoxins into the following classes:
1 The mycotoxin is carcinogenic to humans AFs (Aflatoxins)
2A The mycotoxin is probably carcinogenic to humans –
2B The mycotoxin is possibly carcinogenic to humans AFM1, FBs, OTA, sterigmatocystin
3 The mycotoxin is not classifiable as to its carcinogenicity to humans DON, NIV, PAT, T-2/HT-2, ZEN, citrinin, fusarenon-X
4 The mycotoxin is probably not carcinogenic to humans
Some excerpts from the review:
Toxicity of AFs must be distinguished between acute and chronic. Currently, there is very low incidence of acute AF toxicity in humans. Acute poisoning occurs when the food is contaminated with high concentrations of AFs. This occurs sporadically in developing countries, as happened during the severe acute human aflatoxicosis outbreak in Kenya in 2004, where 317 cases and 125 deaths (39.4% mortality) were reported (Lewis et al., 2005 and Probst et al., 2007). In this case, corn for human consumption was contaminated with AFs levels ranging from 20 to 8000 μg/kg. Acute human poisoning is characterized by vomiting, abdominal pain, pulmonary or cerebral oedema, necrosis, and fatty liver. Other symptoms include anorexia, depression, jaundice, diarrhoea, and photosensitivity. Occurrence of acute aflatoxicosis in animals is more common, as highly contaminated feed is more frequent and susceptibility of livestock species varies.
In human beings, chronic consumption of AF-contaminated foods has been linked to various diseases:
Liver cancer. There is evidence that hepatitis B and/or C viruses and AFs act synergistically in the aetiology of the hepatocellular carcinoma (HCC) (Palliyaguru and Wu, in press and Wu and Santella, 2012). Eastern and South-Eastern Asia and Middle and Western Africa are regions of high HCC incidence. Geographic variations in HCC incidence might be due to geographic differences in the prevalence of various etiological factors, particularly chronic infection with hepatitis viruses, and dietary exposure to AFs.
Effects on the reproductive system. AFs exert negative reproductive effects in human males, causing delayed testicular development, testicular degeneration, decreased reproductive potential, morphological changes, reduced size and weight of the testes, meiotic index decrease, decline in the percentage of live sperm, sperm with increased abnormalities, degeneration of the seminiferous epithelium, and reduced plasma concentration of testosterone, among others (CAST, 2003).
Effects on the immune system. AFs act as immunomodulators, causing a decrease in resistance to secondary infections by fungi, bacteria, and parasites. The cellular response is particularly sensitive to AFs, as evidenced by decreased T or B lymphocyte activity, impaired macrophage/neutrophil effector functions, modified synthesis of inflammatory cytokines, suppressed NK cell-mediated cytolysis, induced reactivation of chronic infection, decreased immunity to vaccination, and impaired immune function in developing animals (Jiang et al., 2008).
Encephalopathy with fatty degeneration of viscera, resembling Reye’s syndrome (Dvorácková et al., 1977). The role of AFs in the development of Reye’s syndrome, which produces fatty degeneration, pale and enlarged liver and kidneys, oedema and stroke has never been unequivocally proved, despite the frequent detection of AFs in the liver of children who have died of this disease and, therefore, is still under discussion.
Pulmonary interstitial fibrosis. In this case, a possible occupational risk of AF exposure via the respiratory tract is suggested (Dvorácková and Píchová, 1986).
On Ochratoxin A:
Regarding OTA, to date there is inadequate evidence of carcinogenicity in humans, but there is sufficient evidence in experimental animals. Therefore, OTA has been classified as possibly carcinogenic to humans (Group 2B) (IARC, 1993). The latest provisional tolerable daily intakes (PTDIs) of this toxin set by the European Food Safety Authority (EFSA, 2006a) and the Joint FAO/WHO Expert Committee on Food Additives (JECFA, 2007) were 17 and 14 ng/kg bw/day, respectively.
The kidney is the major target organ for OTA, recognized as a potent nephrotoxin. In humans, OTA has been identified as the causative agent of nephropathies, often related with urothelial cancer of the upper urinary tract. In animals, OTA intake has also been correlated with an increase in the incidence of testicular cancer. Furthermore, OTA is recognized as teratogenic, genotoxic, carcinogenic, and immunotoxic, but its neurotoxic effect remains unconfirmed.
Chronic effects of OTA are of more concern. In animals, it has been shown that after a prolonged OTA intake, a nephropathy linked to the degeneration of the convoluted tubule of the nephron and renal interstitial fibrosis occurs, followed by a decrease in the thickness of the basal membrane and glomerular hyalinization. Renal lesions observed in birds, pigs, and rodents are very similar. In humans, OTA has been associated with a kidney disease typical of the Balkans, the so-called Balkan Endemic Nephropathy (BEN), mainly present in rural areas of countries like Croatia, Bosnia and Herzegovina, Serbia, Romania, and Bulgaria (Pfohl-Leszkowicz et al., 2002).
Besides renal symptoms, OTA may affect other body systems. It can cross the placenta and has been found to be embryotoxic in rats and mice. animal studies have shown that OTA is immunotoxic; the immunosuppressant activity of OTA in animals is characterized by size reduction of the thymus, spleen, and lymph nodes, depression of antibody responses, changes in immune cells number and function, and modulation of cytokine production. Besides, it has been shown that OTA is associated with cerebellar, hippocampal, and other adverse neurological effects. Finally, OTA has been found in breast milk, which could represent a significant source of exposure for infants (Hope and Hope, 2012).
On Fumonisins
Acute and chronic toxicity by FBs has been largely demonstrated in several animal species, including carcinogenicity and cardiovascular toxic effects (Gelderblom et al., 1988 and Gelderblom et al., 1991). FB1 is a cancer promoter, but a poor cancer initiator.
Currently, there is no direct evidence that FBs cause adverse health effects to humans. Available studies have only shown inconclusive associations between FBs and human cancer. Thus, human exposure to FBs has been associated with oesophageal cancer in South Africa (Sydenham et al., 1990) and liver cancer in China (Yoshizawa et al., 1994).
FBs have also been associated with neural tube defects (NTDs) in the Mexico–Texas border (Missmer et al., 2006). In this case, FBs exposure increased NTDs risk, proportionate to dose, up to a threshold level, at which point foetal death may be more likely to occur. Interestingly, administration of folate may reverse the FBs toxic effect. Thus, FBs-contaminated corn represents a potential risk for human NTD occurrence, especially in populations with inadequate folate intake who rely on corn-based foods (Suarez et al., 2012).
This is getting a bit long, and there are a few others the review mentions: Zearalenone -- some remarks about breast cancer. Trichothecenes (T-2/HT-2, DON) - pneumonia and lung bleeding often followed by death. ** Patulin** - gastrointestinal ulcers, haemorrhages, kidney damage.
I really recommend reading the rest of the review if interested in more details.
What gives me some hope is that the amount of detected mycotoxins seem to be decreasing in developed places, such as the EU, but as the review notes there is more work to do to determine combined exposures from food stuffs that are under individual limits and effects of chronic exposure.